critical care and emergency medicine...critical care and emergency medicine 8 176 recognising the...

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8Critical care and emergency medicine

D.F. TREACHER

I.S. GRANT

Clinical examination of the critically illpatient 176

Provision of critical care 178Organisation of critical care 178Critical care ‘outreach’ 178Admission guidelines 178Transport of the critically ill

patient 179

Monitoring 179General principles 179Monitoring the circulation 179Monitoring respiratory function 182

Physiology of the critically ill patient 182Oxygen transport 182Oxyhaemoglobin dissociation

curve 184Oxygen consumption 184Relationship between oxygen

consumption and delivery 184Pathophysiology of the inflammatory

response 185

Presenting problems in critical illness 186Circulatory failure: ‘shock’ 186Respiratory failure including

ARDS 187Renal failure 189Neurological failure (coma) 189Sepsis 189Disseminated intravascular

coagulation (DIC) 190

General principles of critical caremanagement 190

Management of major organ failure 191Circulatory support 191Respiratory support 193Renal support 197Gastrointestinal and hepatic

support 197Neurological support 198Management of sepsis 199

Discharge from intensive care 200Withdrawal of care 200Brain death 200

Scoring systems in critical care 200

Costs of intensive care 201

Outcome from critical care 201

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C R I T I C A L C A R E A N D E M E R G E N C Y M E D I C I N E

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Recognising the critically ill patient

Full blood countUrea and electrolytes

CreatinineGlucoseArterial blood gas lactateCoagulationCultures: blood, urine, sputumChest X-rayECG

Heart rate; ECGRespiratory rate; SpO2BP—arterial lineTemperatureGCS; pupil size, reactionUrine outputCentral venous pressure

Airway: Support, ? IntubateBreathing: Oxygen Continuous positive airway pressure (CPAP), non-invasive

ventilation (NIV) Intubate and ventilateCirculation: Venous access Fluids Vasoactive drugs

1 Initial assessmentA irway ? Clear

B reathingDistressRateChest movementAuscultation

C irculationPulse: Rate Rhythm VolumeBlood pressure: Direct arterial pressurePeripheral perfusion: Peripheral pulses Temperature Colour Capillary refill

D isabilityConscious level: Glasgow Coma Scale Pupil responses Localising signs

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4

Cardiovascular signs• Cardiac arrest• Pulse rate <40 or >140 bpm• Systolic blood pressure (BP) <100 mmHg• Tissue hypoxia Poor peripheral perfusion Metabolic acidosis Hyperlactataemia• Poor response to volume resuscitation• Oliguria: <0.5 ml/kg/hr (check urea, creatinine, K+)

Respiratory signs• Threatened or obstructed airway• Stridor, intercostal recession• Respiratory arrest• Respiratory rate < 8 or > 35/min• Respiratory ‘distress’: use of accessory muscles; unable to speak in complete sentences• SpO2 < 90% on high-flow O2• Rising PaCO2 > 8 kPa (> 60 mmHg), or > 2 kPa (> 15 mmHg) above ‘normal’ with acidosis

Neurological signs• Threatened or obstructed airway• Absent gag or cough reflex• Failure to maintain normal PaO2 and PaCO2• Failure to obey commands• Glasgow Coma Scale (GCS) < 10• Sudden fall in level of consciousness (GCS fall > 2 points)• Repeated or prolonged seizures

Initial investigations

Monitoring

Immediate management

CLINICAL EXAMINATION OF THE CRITICALLY ILL PATIENT

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C L I N I C A L E X A M I N A T I O N O F T H E C R I T I C A L L Y I L L P A T I E N T

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Intravenous fluidsMonitor displaying blood pressure/right atrial pressure/heart rate/Sp O2

Infusionpumps

Intra-aorticballoon pump

Pacemaker Ventilator(behind

haemofiltrationmachine)

Haemofiltrationmachine

Nitricoxidecylinder

Disseminated intravascular coagulation Bleeding from vessel puncture sites

Skin Haemorrhages and infarcts secondary to disseminated intravascular coagulation

Ischaemia, gangrene secondaryto decreased flow and intravascularcoagulation

Poor urine output

Cold cyanosedperipheries

Tachycardia withlow-volume pulse

Tachypnoea

Confused, unresponsive

Sweating

Reduced conscious level

Multi-organ failureShock

Liver failure with hyperbilirubinaemia

Central nervous system Confusion Coma Intracerebral bleeding

Myocardial depression

Acute respiratory distress syndrome

Gastrointestinal tract Ileus Mucosal damage Haemorrhage Endotoxin leak to portal vein

Hypotension

Meningococcal sepsis: rash

A patient with multi-organ failure supported by haemodynamic monitoring, cardiac pacing, a counterpulsation aortic balloon pump,haemofiltration and nitric oxide therapy.

Some features of shock.

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A critically ill patient is one at imminent risk of death; theseverity of illness must be recognised early and appropriatemeasures taken promptly to assess, diagnose and managethe illness.

The approach required in managing the critically illpatient differs from that required in less severely ill patientswith immediate resuscitation and stabilisation of thepatient’s condition taking precedence:

Priorities are:

● prompt resuscitation, adhering to advanced life supportguidelines (p. 556) and the principles ofcardiorespiratory management explained in this chapter

● urgent treatment of life-threatening emergencies such ashypotension, hypoxaemia, hyperkalaemia,hypoglycaemia and dysrhythmias

● analysis of the deranged physiology● establishing the complete diagnosis in stages as further

history and the results of investigations become available● careful monitoring of the patient’s condition and

response to treatment.

PROVISION OF CRITICAL CARE

ORGANISATION OF CRITICAL CARE

Critical care embraces both intensive care and high-dependency care. Intensive care units (ICUs) are for the care of very ill patients with potential or established organfailure. Initially established for the provision of mechanicalventilation for patients with respiratory failure, ICUs nowmonitor and support all the major organ systems. High-dependency care provides an intermediate level of care at apoint between intensive care and general ward care; it isappropriate both for patients who have had major surgeryand for those with single-organ failure. Ideally the ICUshould be adjacent to the high-dependency unit (HDU),allowing the critical care medical team to manage acombined critical care department.

The intensive care specialist (intensivist) should provide aholistic approach that coordinates expert opinions fromother specialties (surgeons, physicians, microbiologists) toproduce an integrated plan of management that recognisesthe priorities in the treatment of multiple organ failure.

CRITICAL CARE ‘OUTREACH’

Critically ill patients can be found throughout the hospital,in post-operative recovery areas, coronary care units, theacute medical and surgical wards and accident andemergency (A&E) departments. The purpose of ‘outreach’ isto achieve earlier identification of these patients so thatassessment and, if appropriate, transfer to ICU/HDU isarranged before deterioration occurs to the point ofimminent or actual cardiorespiratory arrest. Promptidentification and treatment may even avert the need foradmission to ICU/HDU. Many hospitals are now setting upmedical emergency teams or ‘outreach’/‘patient at risk’

teams (PARTs). In some hospitals the medical emergencyteam may be the cardiac arrest team but with a wider remit, while in others this service is provided by the ICU orHDU team.

Criteria that identify deranged physiology (p. 176) areused to alert the ward nursing and junior medical staff toimpending problems so that they can summon the outreachteam to assess the patient, institute initial resuscitation andsupervise transfer to ICU or HDU as appropriate.

ADMISSION GUIDELINES

Rigid rules to determine admission to ICU/HDU aredestined to fail because every case must be evaluated on itsown merits. Nevertheless, broad guidelines are required to avoid unnecessary suffering and the waste of valuableresources caused by admitting patients who have nothing togain from intensive care because they either are too well orhave no realistic prospect of recovery. The existence of anempty bed does not justify admission. The guiding principlewhen considering ICU/HDU admission should be the timely use of this resource in patients who have a realisticprospect of recovering to achieve a quality of life that theywould value. Patients who do warrant admission should be identified early and admitted without delay since thisimproves survival and reduces the length of stay on the ICU.The wishes of the patient, if known, should be respected andwhatever decision is made should be carefully explained tothe patient’s family.

If the appropriateness of admission remains uncertain, as may occur in the A&E department when little history isavailable, the patient should be given the benefit of the doubtand the indication for continued active treatment reviewedas further information becomes available (Box 8.1).

There is now evidence that for patients undergoing high-risk elective or emergency surgery the mortality,morbidity and both ICU and hospital length of stay arereduced by pre-operative admission to ICU/HDU toimprove cardiorespiratory status (‘pre-optimisation’). Suchpatients are often elderly with cardiorespiratory disease andpoor physiological reserve, and benefit from a protocol ofintensive perioperative care. At present many hospitals havemajor problems in implementing this strategy due to ashortage of critical care beds.

Specific indications for admission to ICU and HDU aregiven in Box 8.2.


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8.1 FACTORS IN THE ASSESSMENT OF A POSSIBLE ICU ADMISSION

● Primary diagnosis and other active medical problems● Prognosis of underlying condition● Severity of physiological disturbance—is recovery still possible?● Life expectancy and anticipated quality of life post-discharge● Wishes of the patient and/or relatives● Availability of the required treatment/technology

N.B. Age alone should not be a contraindication to admission.

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TRANSPORT OF THE CRITICALLY ILLPATIENT

Critically ill patients should be transported to the mostappropriate clinical area for their continuing care. Beforeintra- or inter-hospital transfer is undertaken, the patient’scondition must be stabilised. Appropriate monitoring shouldbe set up and if there is clinical evidence of progressiverespiratory failure or inability to protect the airway,endotracheal intubation and ventilation are indicated.Intubation, while often essential, may be hazardous in thepatient with cardiorespiratory failure, and full monitoringand resuscitation facilities must be available. Hypovolaemiaand hypotension should be corrected and this will oftenrequire monitoring of the central venous pressure (CVP).

Transfer to another hospital may be necessary for furtherinvestigations (such as computed tomography, CT), or tospecialist liver failure, neurosurgical or cardiac surgicalunits. The urgency of providing the specialist treatment hasto be balanced against the stability of the patient’s condition.It may be more appropriate to admit the patient to the localICU for initial stabilisation before transfer. All critically illpatients should be accompanied during transfer by anappropriately trained medical escort.

MONITORING

GENERAL PRINCIPLES

On entering an ICU, relatives, students and even cliniciansmay be intimidated by the numerous tubes and cables

attaching each patient to a battery of ‘alarming’ machines (p. 177). Much of the bedside nurse’s time is spent observing,recording and reacting to the information displayed by thesemonitors, particularly the electrocardiogram (ECG), CVP,arterial blood pressure (BP), temperature and ventilatordata. The trends observed over time, interpreted in relationto changes in therapy, are an important guide to the patient’sprogress.

The critically ill patient should be monitored according tothe following principles:

● Regular clinical examination should never be neglected.● Simple physical signs such as respiratory rate, the

appearance of the patient, restlessness, conscious leveland indices of poor peripheral perfusion (pale, cold skin, delayed capillary refill in the nail bed) are just asimportant as a set of blood gases or numbersimpressively displayed on expensive monitors.

● If there is conflict between clinical assessment and theinformation on a monitor, the monitor should bepresumed to be wrong until all potential sources of errorhave been checked and eliminated. For example, CVPmeasurement may be erroneous because the line isblocked, the system has not been reset to zero after achange in the patient’s position, the tip of the cannula islying in the right ventricle, or another infusion has beenattached to the same central line.

● Changes and trends are more important than any singlemeasurement.

● Many monitors have alarms which will activate if certainmaximum and minimum values are breached. This is acrucial safety feature and may, for example, help toidentify the fact that a patient has become disconnectedfrom the ventilator. Despite the understandable desire toavoid extra noise, the alarm limits should always be setto define physiologically ‘safe’ limits for the variablebeing monitored.

● Sophisticated monitoring systems are often invasive andpose certain hazards, particularly infection (Box 8.3).Always ask ‘Is it necessary?’, and cease monitoring assoon as possible.

MONITORING THE CIRCULATION

Electrocardiogram (ECG)Standard monitors display a single-lead ECG, record heartrate and identify rhythm changes. More sophisticatedmachines can print out rhythm strips and monitor STsegment shift, which may be useful in patients withischaemic heart disease.

Blood pressureThis may be measured intermittently using an automatedsphygmomanometer but in critically ill patients continuousintra-arterial monitoring, using a line placed in the radialartery, is preferable. It is important to appreciate that whenthere is systemic vasoconstriction the mean arterial pressuremay be normal or even high although the cardiac output islow. Conversely, if there is peripheral vasodilatation, as in

M O N I T O R I N G

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8.2 ADMISSION CRITERIA FOR ICU AND HDU

Admission to ICU

● Patients requiring or likely to require endotracheal intubation andinvasive mechanical ventilatory support

● Patients requiring support of two or more organ systems (e.g.inotropes and haemofiltration)

● Patients with chronic impairment of one or more organ systems(e.g. chronic obstructive pulmonary disease (COPD) or severeischaemic heart disease (IHD)) who also require support for acutereversible failure of another organ system

Admission to HDU

● Patients who require far more detailed observation or monitoringthan can be safely provided on a general ward

Direct arterial blood pressure (BP) monitoringCentral venous pressure (CVP) monitoringFluid balanceNeurological observations, regular Glasgow Coma Scale (GCS) recording

● Patients requiring support for a single failing organ system butexcluding invasive ventilatory support

Mask continuous positive airway pressure (CPAP) ornon-invasive (mask) ventilation (NIPPV)—Box 8.17, page 193Low- to medium-dose inotropic supportRenal replacement therapy in an otherwise stable patient

● Patients no longer requiring intensive care but who cannot besafely managed on a general ward

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sepsis, the mean arterial pressure may be low although thecardiac output is high.

Central venous pressure (CVP)CVP or right atrial pressure (RAP) is monitored using acatheter inserted via either the internal jugular or thesubclavian vein with the distal end sited in the upper rightatrium. Although on general wards and some HDUsmeasurements may be made using a saline-filled manometertube, in ICU the line is transduced as for arterial pressuremeasurement. The zero reference point used is normally themid-axillary line (MAL), which approximates to the level ofthe tricuspid valve or mid-right atrium with the patient lyingsemi-supine. All intravascular pressures quoted in thischapter are referenced to that point. The classical bedsideclinical examination uses the ‘sternal angle’ as the zeroreference point and this lies approximately 6–8 cm(depending on the antero-posterior chest diameter)vertically above MAL. (Values of CVP measured from thisreference point will therefore be 6–8 cm lower than valuesrecorded from MAL.)

The CVP is a useful means of assessing the need forintravascular fluid replacement and the rate at which itshould be given. If the CVP is low in the presence of a lowmean arterial pressure (MAP) or cardiac output, fluidresuscitation is necessary. However, a raised level does notnecessarily mean that the patient is adequately volumeresuscitated. It must be remembered that right heartfunction, pulmonary artery pressure, intrathoracic pressureand venous ‘tone’ also influence CVP and may lead to araised CVP even when the patient is hypovolaemic. Inaddition, positive pressure ventilation raises intrathoracicpressure and causes marked swings in atrial pressures andsystemic blood pressure in time with respiration. Pressuremeasurements should be recorded at end-expiration or, ifsafe, off the ventilator because these values provide the mostreliable measure of ventricular end-diastolic transmuralpressure.

In severe hypovolaemia the RAP may be sustained byperipheral venoconstriction, and transfusion may initiallyproduce little or no change in the CVP (Fig. 8.1).

Pulmonary artery ‘wedge’ pressure (PAWP)and PA catheterisationIn most situations the CVP is an adequate guide to the fillingpressures of both sides of the heart; however, certainconditions such as pulmonary hypertension or rightventricular dysfunction may lead to raised CVP levels evenin the presence of hypovolaemia. If this is suspected, it maybe appropriate to insert a pulmonary artery flotation catheter(Fig. 8.2) so that pulmonary artery pressure and PAWP,which approximates to left atrial pressure, can be measured.The mean PAWP normally lies between 8 and 12 mmHg(measured from the mid-axillary line) but in left heart failureit may be grossly elevated and even exceed 30 mmHg.Provided the pulmonary capillary membranes are intact, theoptimum PAWP when managing acute circulatory failure inthe critically ill patient is generally 12–15 mmHg becausethis will ensure good left ventricular filling without riskinghydrostatic pulmonary oedema.

These catheters may also be used to measure cardiacoutput, sample blood from the pulmonary artery (‘mixedvenous’ samples) and, by oximetry, provide continuousmonitoring of the mixed venous oxygen saturation (SvO2).Measurement of SvO2 gives an indication of the adequacy ofcardiac output in relation to the body’s metabolic require-ments and is especially useful in low cardiac output states.

Cardiac outputThe most widely used method for cardiac output measure-ment is the thermodilution technique using a PA catheter. Abolus of cold 5% dextrose is rapidly injected into the rightatrium via the CVP line and mixes with the total venousreturn in the right ventricle, producing a drop in thepulmonary artery temperature that is sensed by a thermistorat the tip of the PA catheter. The cardiac output is derivedfrom the volume and temperature of the injectate and theresulting change in temperature measured in the pulmonary


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8.3 COMPLICATIONS AND PITFALLS OF CENTRAL VENOUS AND PULMONARY ARTERY (PA) CANNULATION

At insertion

● Pneumothorax—more likely with subclavian than with internaljugular approach

● Haematoma from accidental arterial puncture● Air embolism● Dysrhythmia● Damage to thoracic duct with left internal jugular or subclavian

approach● Knotting of catheter*● Pulmonary artery rupture*

In situ

● Sepsis● Endocarditis● Thrombosis● Pulmonary infarct*● Pulmonary artery rupture*● Erroneous information● Inappropriate response to information

* Risk associated specifically with PA catheterisation.

HypervolaemiaNormovolaemiaHypovolaemia

CVP

0 3015Time (min)

Fig. 8.1 The different responses observed in central venouspressure (CVP) after a fluid challenge of 250 ml, depending on theintravascular volume status of the patient.

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artery; it is inversely related to the area under thetemperature–time curve. Although generally viewed as the‘gold standard’ for clinical measurement of cardiac output,the error may be 10–15%.

Thermodilution cardiac output measurement has beenrefined by the development of PA catheters incorporating aheating element, which raises blood temperature at frequentintervals, with the resultant temperature change alsodetected by the thermistor. These ‘continuous’ cardiacoutput catheters dispense with the need for injections of colddextrose.

Increasingly less invasive methods for monitoring cardiacoutput are being used, such as oesophageal Dopplerultrasonography. This involves inserting a 6 mm probe intothe distal oesophagus to allow continuous monitoring of the aortic flow signal from the descending aorta (Fig. 8.3).From the stroke distance (area under velocity/timewaveform), and using a correction factor that incorporatesthe patient’s age, height and weight, an estimate of leftventricular stroke volume and hence cardiac output can bemade. Peak velocity is an indicator of left ventricularperformance while flow time is an indicator of leftventricular filling and peripheral resistance. OesophagealDoppler provides a rapid and clinically useful assessment ofvolume status and cardiac performance to guide early fluidand vasoactive therapy.

Analysis of arterial pressure waveform is another meansof continuously estimating cardiac output, and can be cali-brated either by transpulmonary thermodilution (PiCCO) orlithium dilution methods (LidCO).

Urine outputThis is a sensitive measure of renal perfusion, provided thatthe kidneys are not damaged (e.g. acute tubular necrosis) oraffected by drugs (e.g. diuretics, dopamine), and can bemonitored accurately if a urinary catheter is in place. It is

M O N I T O R I N G

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30

20

10

0

mmHg

Rightventricularpressure

Wedge(left atrial)pressure

Ballooninflated

RV

RA

LA

LV

Aorta

Balloon

Pulmonaryartery

Right atrialpressure

Pulmonaryartery

pressure

A

B

Fig. 8.2 A pulmonary artery catheter. A There is a small balloon at the tip of the catheter and pressure can be measured through the centrallumen. The catheter is inserted via an internal jugular, subclavian or femoral vein and advanced through the right heart until its tip lies in thepulmonary artery. When the balloon is deflated the pulmonary artery pressure can be recorded. B Advancing the catheter while inflating the balloonwill ‘wedge’ the catheter in the pulmonary artery. In this position blood cannot flow past the balloon so the tip of the catheter will now record thepressure transmitted from the pulmonary veins and left atrium. This is known as the pulmonary artery wedge pressure and provides an indirectmeasure of the left atrial pressure.

Fig. 8.3 Oesophageal Doppler ultrasonography.

OesophagealDoppler probe

Strokedistance

Peakvelocity

Flowtime

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normally measured hourly and the lower limit of normal is 0.5 ml/hr/kg body weight.

Fluid balanceAssessing fluid balance in critically ill patients is a difficultbut important discipline. Weighing the patient daily can behelpful but is extremely difficult, and assessment is usuallybased on fluid balance charts which record:

● inputs: oral, nasogastric and intravenous, classified ascrystalloid and colloid

● outputs: urine, nasogastric, fistulae, vomiting, diarrhoeaand surgical drain losses.

The insensible loss from skin, respiration etc. is normally500–1000 ml/day but can exceed 2 litres/day in a pyrexialpatient with open wounds.

Peripheral/skin temperatureThis is conventionally measured over the dorsum of the foot and reflects cutaneous blood flow and venous filling.The gradient between peripheral and central or ‘core’temperature (from rectal, oesophageal or tympanic probes)may be used to assess peripheral perfusion; a difference of< 3°C suggests that both intravascular fluid replacement andtissue perfusion are adequate.

Blood lactate, hydrogen ion and base deficitA metabolic acidosis with base deficit > 5 mmol/l requiresexplanation (p. 437). It often indicates increased lactic acidproduction in poorly perfused, hypoxic tissues and impairedlactate metabolism due to poor hepatic perfusion. Seriallactate measurements may therefore be helpful in moni-toring tissue perfusion and the response to treatment. Otherconditions such as acute renal failure, ketoacidosis andpoisoning may be the cause (p. 438). Large volumeinfusions of fluids containing sodium chloride, e.g. in theatreor during resuscitation, may lead to a hyperchloraemicacidosis.

MONITORING RESPIRATORY FUNCTION

Oxygen saturation (SpO2)This is measured by a probe, usually attached to a finger orearlobe. Spectrophotometric analysis is used to determinethe relative proportions of saturated and desaturatedhaemoglobin. The technique is unreliable if peripheralperfusion is poor and may produce erroneous results in the presence of nail polish, excessive movement or highambient light. In general, arterial oxygenation is satisfactoryif SpO2 is greater than 90%. In the ICU, sudden falls in SpO2

may be caused by:

● pneumothorax● displacement of the endotracheal tube● disconnection from the ventilator● lung collapse due to thick secretions blocking the

proximal bronchial tree● circulatory collapse causing a poor signal due to

impaired peripheral perfusion● error such as a detached probe.

Arterial blood gasesThese are usually measured several times a day in aventilated patient so that inspired oxygen (FIO2) and minutevolume can be adjusted to achieve the desired PaO2 andPaCO2 respectively. Analysis of arterial blood gas results isalso a useful means of monitoring disturbances of acid–basebalance (Ch. 16).

Lung functionIn ventilated patients lung function is monitored by:

● alveolar–arterial PO2 gradient and hypoxaemia index(PaO2/FIO2), both measures of gas exchange

● arterial and end-tidal CO2, reflecting alveolar ventilation

● tidal volume (VT), respiratory rate (f), minute volume(VT × f), airway pressure and compliance, reflectingairways resistance, the ‘stiffness’ of the lungs and theease with which the patient can meet the required workof breathing.

CapnographyThe CO2 concentration in inspired gas is zero, but duringexpiration, after clearing the physiological dead space, itrises progressively to reach a plateau which represents thealveolar or end-tidal CO2 concentration. This cyclical changein CO2 concentration or capnogram is measured using aninfrared sensor inserted between the ventilator tubing andthe endotracheal tube. With normal lungs, the end-tidal CO2 closely mirrors PaCO2, and can be used to assess theadequacy of alveolar ventilation. However, there may beconsiderable discrepancies if there is lung disease or impairedpulmonary perfusion (for example, due to hypovolaemia).Trends in end-tidal CO2 are useful in head injury manage-ment and during the transport of ventilated patients.

In combination with the gas flow and respiratory cycle data from the ventilator, CO2 production and hencemetabolic rate may be calculated.

PHYSIOLOGY OF THE CRITICALLY ILL PATIENT

OXYGEN TRANSPORT

The major function of the heart, lungs and circulation is the provision of oxygen and other nutrients to the variousorgans and tissues of the body. During this process carbondioxide and the other waste products of metabolism areremoved. The rate of supply and removal should match thespecific metabolic requirements of the individual tissues.This requires adequate oxygen uptake in the lungs, globalmatching of delivery and consumption, and regional controlof the circulation. Failure to supply sufficient oxygen tomeet the metabolic requirements of the tissues is thecardinal feature of circulatory failure or ‘shock’.

The transport of oxygen from the atmosphere to themitochondria within individual cells is illustrated in Figure8.4. The important points to note are that:


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● The movement of oxygen from pulmonary capillary tosystemic tissue capillary, referred to as the globaloxygen delivery (DO2), relies on convection or bulk flowand is the product of cardiac output and arterial oxygencontent.

● The regional distribution of oxygen delivery is vital. Ifskin and muscle receive high blood flows but thesplanchnic bed does not, the gut will become hypoxiceven if overall oxygen delivery is high.

● The major determinants of the oxygen content of arterialblood (CaO2) are the arterial oxygen saturation ofhaemoglobin (SaO2) and the haemoglobin concentration(over 95% of oxygen carried in the blood is attached tohaemoglobin). The shape of the oxyhaemoglobindissociation curve dictates that increases in PaO2 beyondthe level that ensures SaO2 is > 90% produce relativelysmall additional increases in CaO2 (Fig. 8.5). Consider a

patient who is both anaemic (Hb 60 g/l) and hypoxaemic(SaO2 75%) when breathing air (FIO2 0.21).Supplementary oxygen at FIO2 0.4 will increase SaO2 to93%; CaO2 will increase by 24% but further increases inFIO2 while increasing PaO2 cannot produce any furtheruseful increases in SaO2 or CaO2. However, increasingHb to 90 g/l by blood transfusion will result in a further50% increase in CaO2.

● The movement of oxygen from tissue capillary to celloccurs by diffusion and depends on the gradient ofoxygen partial pressures, diffusion distance and theability of the cell to take up and use oxygen. Thereforemicrocirculatory, tissue diffusion and cellular factors, aswell as DO2, influence the oxygen status of the cell.

● Supranormal levels of oxygen delivery cannotcompensate for diffusion problems between capillaryand cell, nor for metabolic failure within the cell.

P H Y S I O L O G Y O F T H E C R I T I C A L L Y I L L P A T I E N T

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= 200ml O2/l = 1.36ml O2/gram of 100% saturated Hb = 3ml/l = 1000ml/min = 250ml/min = 25%

P lO2 humidified (20)P lO2 dry (21)

PEO2 (15.9)PECO2 (4.2)

Expired dryVi/e (5)

Heart andlungs

PAO2(14)

Calculations

PvO2(5.3)

P50 SvO2 (75)Hb (150)

CvO2 (150)QT (5)

O2R(750)

Mitochondrial PO2(1.3–0.7)

Intracellular PO2(2.7–1.3)

Interstitial PO2(5.3–2.7)

Capillary PO2

VCO2(200)

VO2(250)

DO2(1000)

Venous(5.3)

Arterial(13)

Diffusion of O2 in tissues

CaO2 (200)QT (5)

SaO2 (97)Hb (150)

PaO2(13)

P50

(3.5)

‘Shunt’(2–3%)

CaO2

kPaO2 x 0.23

DO2

VO2

OER

= (Hb x k x SaO2/100) + (PaO2 x 0.23) = coefficient of haemoglobin oxygen-binding capacity = oxygen dissolved in plasma = QT x CaO2

= VO2/DO2 x 100 = QT (CaO2–CVO2)

Fig. 8.4 Transport of oxygen from inspired gas to the cell, demonstrating the ‘oxygen cascade’, with equations for calculation of arterialoxygen content, global oxygen delivery, consumption and extraction. Values in parentheses for a normal 70 kg individual (body surface area:1.67 m2) breathing air (F IO2: 0.21) at standard atmospheric pressure (PB: 101 kPa). Partial pressures of O2, CO2 in kPa; saturation in %; contents(CaO2, Cv O2) in ml/litre; Hb in g/l; blood/gas flows (QT, Vi/e) in litre/min; oxygen transport (DO2, O2R), VO2 and V CO2 in ml/min. To convert kPa tommHg, multiply by 7.5.CaO2 = arterial O2 content O2R= oxygen return P IO2 = inspired PO2 SO2=oxygen saturation (%)CvO2 = mixed venous O2 content PaO2= arterial PO2 PO2 = oxygen partial pressure (kPa) SvO2 = mixed venous SO2

DO2 = oxygen delivery PAO2 = alveolar PO2 PvO2 = venous PO2 V CO2 = CO2 productionHb = haemoglobin PECO2= mixed expired PCO2 QT = cardiac output Vi/e= minute volume: inspired/expiredOER = oxygen extraction ratio PEO2 = mixed expired PO2 SaO2 = arterial SO2 VO2 = oxygen consumption

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OXYHAEMOGLOBIN DISSOCIATION CURVE

The oxyhaemoglobin dissociation curve (Fig. 8.5) describesthe relationship between the saturation of haemoglobin(SO2) and the partial pressure (PO2) of oxygen in the blood.Due to the shape of the curve, a small drop in PaO2 below8 kPa (60 mmHg) will cause a marked fall in SaO2. Itsposition and the effect of various physico-chemical factorsare defined by the PO2 at which 50% of the haemoglobin issaturated (P50), which is normally 3.5 kPa (26 mmHg).

A shift in the curve will influence the uptake and releaseof oxygen by the Hb molecule; for example, if the curvemoves to the right, the haemoglobin saturation will be lowerfor any given oxygen tension and therefore less oxygen willbe taken up in the lungs but more will be released to thetissues. As capillary PCO2 rises, the curve moves to the right,increasing unloading of oxygen in the tissues—a phenomenonknown as the Bohr effect.

Traditionally, the optimum haemoglobin concentrationfor critically ill patients had been considered to beapproximately 100 g/l, representing a balance betweenmaximising the oxygen content of the blood and avoidingregional microcirculatory problems due to increasedviscosity. However, recent evidence suggests an improvedoutcome in critically ill patients if the haemoglobinconcentration is maintained between 70 and 90 g/l, with theexception of the elderly and patients with coronary arterydisease, in whom a level of 100 g/l remains appropriate.

OXYGEN CONSUMPTION

The sum of the oxygen consumed by the various organsrepresents the global oxygen consumption (VO2) and is

approximately 250 ml/min for an adult of 70 kg undertakingnormal daily activities. VO2 may be calculated indirectlyfrom the product of cardiac output and the arterial mixedvenous oxygen content difference (CaO2–CvO2), as shownin Figure 8.4, or directly by sampling the inspired andmixed-expired gases from the ventilator and measuringinspired and expired minute volume using either a massspectrometer or metabolic cart.

The oxygen saturation in the pulmonary artery, otherwiseknown as the mixed venous oxygen saturation (SvO2),represents a measure of the oxygen not consumed by thetissues (DO2–VO2). The saturation of venous blood fromdifferent organs varies considerably; for example, thehepatic venous saturation usually does not exceed 60% but the renal venous saturation may reach 90%, reflectingthe great difference in both the metabolic requirements of these organs and the oxygen content of the blooddelivered to them. The SvO2 is influenced by changes both in oxygen delivery (DO2) and consumption (VO2) and,provided the microcirculation and the mechanisms forcellular oxygen uptake are intact, can be used to monitorwhether global oxygen delivery is adequate to meet overalldemand.

The reoxygenation of the blood that returns to the lungsand the resulting arterial saturation (SaO2) will depend onhow closely pulmonary ventilation and perfusion arematched. If part of the pulmonary blood flow perfuses non-ventilated parts of the lung, there will be ‘shunting’,and the blood entering the left atrium will be desaturated in proportion to the size of this shunt and the level of SvO2.

RELATIONSHIP BETWEEN OXYGENCONSUMPTION AND DELIVERY

The tissue oxygen extraction ratio (OER), which is 20–25%in a normal subject at rest, rises as consumption increases or supply diminishes (Fig. 8.6). The maximum OER isapproximately 60% for most tissues; at this point no furtherincrease in extraction can occur and any further increase in oxygen consumption or decline in oxygen delivery willcause tissue hypoxia, anaerobic metabolism and increasedlactic acid production.

In sepsis the slope of maximum OER decreases,reflecting the reduced ability of tissues to extract oxygen(DE cf. AB on Fig. 8.6), but the curve does not plateau and oxygen consumption continues to increase even at‘supranormal’ levels of oxygen delivery. This conceptencouraged some physicians to treat septic shock usingvigorous intravenous fluid loading and inotropic support,usually with dobutamine, with the aim of achieving veryhigh oxygen deliveries (> 600 ml/min/m2) in the belief that this strategy would increase oxygen consumption,relieve tissue hypoxia, prevent multiple organ failure andimprove prognosis. Trials have demonstrated no benefit inICU patients with established organ failure but suggest thatit may be worthwhile if applied before organ failuresupervenes (Box 8.4)


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Hae

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tion

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13121110987654321

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80

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P50

TemperatureH+

PaCO2

2,3 DPG

Fig. 8.5 The relationship between oxygen tension (PO2) andpercentage saturation of haemoglobin with oxygen (SO2). Thedotted line illustrates the rightward shift of the curve (i.e. P50 increases)caused by increases in temperature, PaCO2, metabolic acidosis and 2,3 diphosphoglycerate (DPG).

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PATHOPHYSIOLOGY OF THEINFLAMMATORY RESPONSE

The mediators and clinical manifestations of the inflam-matory response are described on pages 75–76. In critically ill patients these processes have important consequences(Box 8.5).

Fever, tachycardia with warm peripheries, tachypnoeaand a raised white cell count traditionally prompt a diag-nosis of sepsis with the implication that the clinical pictureis caused by invading microorganisms and their breakdownproducts. However, other conditions such as pancreatitis,trauma, malignancy, tissue necrosis, aspiration syndromes,liver failure, blood transfusion and drug reactions can allproduce the same clinical picture in the absence of infection.

Local inflammationThe body’s initial response to a noxious local insult is toproduce a local inflammatory response with sequestrationand activation of white blood cells and the release of avariety of mediators to deal with the primary ‘insult’ andprevent further damage either locally or in distant organs.

Normally, a delicate balance is achieved between pro- andanti-inflammatory mediators. However, if the inflammatoryresponse is excessive, local control is lost and a large arrayof mediators including prostaglandins, leukotrienes, free

oxygen radicals and particularly pro-inflammatory cytokines(p. 66) are released into the circulation.

The inflammatory and coagulation cascades areintimately related. The process of blood clotting not onlyinvolves platelet activation and fibrin deposition but alsocauses activation of leucocytes and endothelial cells.Conversely, leucocyte activation induces tissue factorexpression and initiates coagulation. Control of thecoagulation cascade is achieved through the natural anti-coagulants antithrombin (AT) III, activated protein C (APC)and tissue factor pathway inhibitor (TFPI) which not onlyregulate the initiation and amplification of the coagulationcascade but also inhibit the pro-inflammatory cytokines.Deficiency of ATIII and APC (features of disseminatedintravascular coagulation (DIC), see below) facilitatesthrombin generation and promotes further endothelial celldysfunction.

Systemic inflammationDuring a severe inflammatory response systemic release of cytokines and other mediators triggers widespreadinteraction between the coagulation pathways, platelets,endothelial cells and white blood cells, particularly thepolymorphonuclear cells (PMNs). These ‘activated’ PMNs

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Oxygenconsumption(VO2) ml/min

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8.4 EARLY GOAL-DIRECTED THERAPY IN SEVERE SEPSIS

‘In patients with severe sepsis or septic shock managed initially inA&E, early goal-directed therapy (EGT) reduced 60-day mortalityfrom 57% to 44%. Both groups were resuscitated with similartargets for CVP, arterial blood pressure and urine output, but in theEGT group additional goals were central venous oxygen saturation > 70% and haematocrit > 30%, resulting in more rapid fluidresuscitation and higher RBC transfusion rates in the first 6 hours.’● Rivers E, et al. N Engl J Med 2001; 345:1368–1377.

EBM

Fig. 8.6 The effects of changing oxygen delivery on consumption.The solid line (ABC) represents the normal relationship and the dottedline (DEF) the altered relationship believed to exist in sepsis.

8.5 TERMINOLOGY USED TO DESCRIBE THE INFLAMMATORY STATE

Infection

● Invasion of normally sterile host tissue by microorganisms

Bacteraemia

● Viable bacteria in the blood

Systemic inflammatory response syndrome (SIRS)

● Encompasses inflammatory response to both infective and non-infective causes such as pancreatitis, trauma,cardiopulmonary bypass, vasculitis etc.

● Defined by presence of two or more of:Temperature > 38.0°C or < 36.0°CHeart rate > 90/minRespiratory rate > 20/minPaCO2 < 4.3 kPa (< 32 mmHg) or ventilatedWhite blood count > 12 × 109/l or < 4 × 109/l

Sepsis

● Systemic inflammatory response caused by documented infection

Severe sepsis/SIRS

● Sepsis/SIRS with evidence of early organ dysfunction orhypotension

Septic/SIRS shock

● Sepsis associated with organ failure and hypotension (systolic BP < 90 mmHg or > 40 mmHg fall from baseline) unresponsiveto fluid resuscitation

Multiple organ dysfunction syndrome (MODS)

● Development of impaired organ function in critically ill patientswith SIRS

● If prompt treatment of underlying cause and suitable organ supportare not achieved, then multiple organ failure (MOF) will ensue

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express adhesion factors (selectins) causing them initially toadhere to and roll along the endothelium, then to adherefirmly and finally to migrate through the damaged anddisrupted endothelium into the extravascular, interstitialspace together with fluid and proteins, resulting in tissueoedema and inflammation. A vicious circle of endothelialinjury, intravascular coagulation, microvascular occlusion,tissue damage and further release of inflammatorymediators ensues.

All organs may become involved. This manifests in thelungs as the acute respiratory distress syndrome (ARDS)and in the kidneys as acute tubular necrosis (ATN), whilewidespread disruption of the coagulation system results in the clinical picture of DIC.

The endothelium itself produces mediators that locallycontrol blood vessel tone: endothelin 1, a potent vaso-constrictor, and prostacyclin and nitric oxide (NO, p. 76)which are systemic vasodilators. NO (which is alsogenerated outside the endothelium) is implicated in both themyocardial depression and the profoundly vasodilatedcirculation (both arterioles and venules) that causes therelative hypovolaemia and systemic hypotension found inseptic/SIRS shock.

A major component of the tissue damage in septic/SIRSshock is the inability to take up and use oxygen atmitochondrial level even if global oxygen delivery issupranormal. This effective bypassing of the tissues resultsin a reduced arteriovenous oxygen difference, a low oxygenextraction ratio, a raised plasma lactate and a paradoxicallyhigh mixed venous oxygen saturation (SvO2).

If both the precipitating cause and accompanyingcirculatory failure (hypotension and frequently severe

hypovolaemia due to venodilatation and fluid loss throughthe leaky vascular endothelium) are promptly controlledbefore significant organ failure occurs (‘early’ shock), theprognosis is good. However, if the global and peripheralcirculatory failure is not corrected promptly, and particularlyif the underlying cause is not effectively treated, progressivedeterioration in organ function occurs and multiple organfailure (MOF) ensues (‘late’ shock).

The mortality of MOF is high and increases with thenumber of organs that have failed, the duration of organfailure and the patient’s age. Failure of four or more organsis associated with a mortality > 80%.

PRESENTING PROBLEMS IN CRITICAL ILLNESS

CIRCULATORY FAILURE: ‘SHOCK’

Circulatory failure or ‘shock’ exists when the oxygendelivery (DO2) fails to meet the metabolic requirements ofthe tissues. In the context of critical illness, ‘shock’ is oftenconsidered to be synonymous with hypotension and todefine the state of circulatory failure. While hypotension isa sinister development and requires urgent attention, it ismost important to appreciate that hypotension is often a latemanifestation of circulatory failure or shock and that thecardiac output and oxygen delivery may be critically loweven though the blood pressure remains normal (Box 8.6);the problem should be identified and treatment institutedbefore the blood pressure falls.


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8.6 TYPICAL CIRCULATORY MEASUREMENTS IN A NORMAL ADULT AND IN VARIOUS CARDIORESPIRATORY CONDITIONS THAT MAY CAUSE CIRCULATORY ‘SHOCK’

RAP/CVP LAP/PAWP PAP MAP Heart rate Cardiac CaO2 DO2Clinical condition (mmHg) (mmHg) (mmHg) (mmHg) (/min) output (l/min) SVR* PVR* (ml/l) (ml/min)

Normal 6 11 16 96 70 5 18 1 200 1000

Major haemorrhage 0 4 11 81 120 3 27 2.3 160 480

Left heart 8 20 24 96 100 3.7 24 1 180 670failure

Major pulmonary 12 6 36 81 110 2.5 28 12 160 400embolism

Exacerbation of 11 10 42 82 100 6 12 5 150 900COPD

Septic shockPre-volume load 3 8 16 55 130 4.5 12 1.3 150 675Post-volume load 9 15 23 60 120 7.5 7 1.1 140 1050

* Multiply by 80 to give SI units: dyn.sec/cm5. To adjust for the size of the patient, the measurements of flow and resistance are frequently indexedby dividing by the patient’s body surface area.

(RAP/LAP = right/left atrial pressure; CVP = central venous pressure; PAWP = pulmonary artery wedge pressure; PAP/MAP = pulmonaryartery/mean arterial pressure; SVR/PVR = systemic/pulmonary vascular resistance; CaO2 = arterial oxygen content; DO2 = global oxygen delivery;COPD = chronic obstructive pulmonary disease)

Note These values are merely examples. The severity of the condition and pre-existing cardiorespiratory disease will affect the precise figuresobtained in individual cases. Note that in contrast to other conditions the oxygen delivery is high in septic shock after volume loading. When thecirculatory abnormalities have been defined in this way, appropriate management may be planned.

Pressures quoted referenced to zero at mid-axilla as is usual practice in ICU. Subtract vertical distance from mid-axilla to sternal angle (approx.6–8 mmHg) if sternal angle used as reference point.

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The many causes of circulatory failure or ‘shock’ maybroadly be classified into:

● hypovolaemic—any condition provoking a majorreduction in blood volume, e.g. internal or externalhaemorrhage, severe burns, dehydration

● cardiogenic—any form of severe heart failure, e.g.myocardial infarction, acute mitral regurgitation

● obstructive—obstruction to blood flow around thecirculation, e.g. major pulmonary embolism, cardiactamponade, tension pneumothorax

● neurogenic—caused by major brain or spinal injuryproducing disruption of brain stem and neurogenicvasomotor control; may be associated with neurogenicpulmonary oedema

● anaphylactic—inappropriate vasodilatation triggered byan allergen (e.g. bee sting)

● septic/SIRS—infection or other causes of a systemicinflammatory response that produce widespreadendothelial damage with vasodilatation, arteriovenousshunting, microvascular occlusion and tissue oedema,resulting in organ failure.

Clinical assessment and complicationsAlthough dependent to some extent on the underlying cause,a range of clinical features are common to most cases(Box 8.7 and p. 177).

Hypovolaemic, cardiogenic and obstructive causes ofcirculatory failure produce the ‘classical’ image of shock,with cold peripheries, weak central pulses and evidence of alow cardiac output. In contrast, neurogenic, anaphylacticand septic shock are usually associated with warmperipheries, bounding pulses and features of a high cardiac

output. The central venous pressure (jugular venouspressure, JVP) is typically reduced in hypovolaemic andanaphylactic shock but elevated in cardiogenic andobstructive shock, and may be low, normal or high inneurogenic and septic shock. This is an important distinctionand direct measurement of the CVP or PAWP (Fig. 8.2,p. 181) may be very helpful if the physical signs are difficultto interpret. Figure 8.7 indicates how the likely diagnosismay be established by careful analysis of the CVP,peripheral perfusion, pulse volume and haematocrit. Allforms of shock require early identification and treatmentbecause, if inadequate regional tissue perfusion and cellulardysoxia persist, multiple organ failure will develop.

RESPIRATORY FAILURE INCLUDING ARDS

The majority of patients admitted to ICU/HDU will haverespiratory problems either as the primary cause of theiradmission or secondary to pathology elsewhere. Respiratoryfailure is formally classified on the basis of blood gasanalysis into:

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Myocardial infarctPulmonary embolus

Tensionpneumothorax

Cardiac tamponadeSepsis

SepsisCO2 retention

Over-transfusion

SepsisAnaphylaxis

Drugs/overdoseCNS lesions

GI tractTrauma

Major vesselThorax

AbdomenRetroperitoneal

GI tractAscitesRenalSepsis

Normal Normalor reduced

Normalor increased

Normalor reduced Increased

Haemorrhage Na/H2O lossDiagnosesto consider

Haematocrit

Reduced Increased Increased ReducedPulse volume

Cold Warm Warm ColdPeripheraltemperature

Raised Low

Measure CVP(mmHg from mid-axillary line)

Fig. 8.7 A guide to the initial analysis and diagnosis of circulatory shock.

8.7 GENERAL FEATURES OF SHOCK

● Hypotension (systolic BP < 100 mmHg)● Tachycardia (> 100/min)● Cold, clammy skin● Rapid, shallow respiration● Drowsiness, confusion, irritability● Oliguria (urine output < 30 ml/hr)● Elevated or reduced central venous pressure (see text)● Multi-organ failure

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● type 1—hypoxaemia (PaO2 < 8 kPa (< 60 mmHg) whenbreathing air) without hypercapnia caused by a failure ofgas exchange due to mismatching of pulmonaryventilation and perfusion

● type 2—hypoxaemia with hypercapnia (PaCO2 > 6.5 kPa(> 49 mmHg)) due to alveolar hypoventilation whichoccurs when the respiratory muscles cannot performsufficient effective work to clear the carbon dioxideproduced by the body.

Although this distinction is conceptually useful, it cannotbe applied too rigidly in critically ill patients since they may change from type 1 to 2 as their illness progresses. For example, hypercapnia may develop in pneumonia orpulmonary oedema as the patient tires and can no longersustain the increased work of breathing.

Pulmonary problems in critically ill patients can also beclassified according to the functional residual capacity(FRC, or the lung volume at the end of expiration).Examples of low FRC include lung collapse, pneumonia andpulmonary oedema; examples of a high FRC (i.e. over-distended lungs) include asthma, COPD and bronchiolitis.This allows logical management directed at improving lungcompliance and reducing the work of breathing.

The more common causes of acute respiratory failurepresenting to ICU/HDU for respiratory support are shown inBox 8.8.

The presentation, differential diagnosis and initialtreatment of the primary respiratory conditions causingacute respiratory failure are covered in Chapter 19.

The assessment of respiratory failure in the critically illpatient should be guided by several important principles:

● The patient’s appearance (tachypnoea, difficultyspeaking in complete sentences, laboured breathing,exhaustion, agitation or increasing obtundation) is more important than measurement of blood gases in deciding when it is appropriate to provide mechanical respiratory support or intubation.

● Adequate supplemental oxygen to maintain SpO2 > 94%should be provided. If the inspired oxygen concentrationrequired exceeds 0.6, refer to the critical care team.

● Monitoring of SpO2 and arterial blood gases is helpful indocumenting progress.

● Restless patients dependent on supplementary oxygen or with deteriorating conscious level are at risk. If theyremove the mask or vomit, the resulting hypoxaemia oraspiration may be catastrophic.

● An attempt should be made to reduce the work ofbreathing, e.g. by treating bronchoconstriction or usingCPAP (Box 8.17, p. 193).

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

This describes the acute, diffuse pulmonary inflammatoryresponse to either direct (via airway or chest trauma) orindirect blood-borne insults that originate from extra-pulmonary pathology. It is characterised by neutrophilsequestration in pulmonary capillaries, increased capillarypermeability, protein-rich pulmonary oedema with hyalinemembrane formation, damage to type 2 pneumocytesleading to surfactant depletion, alveolar collapse andreduction in lung compliance. If this early phase does not resolve with treatment of the underlying cause, a fibroproliferative phase ensues and causes progressivepulmonary fibrosis. It is frequently associated with otherorgan dysfunction (kidney, heart, gut, liver, coagulation) aspart of multiple organ failure. The term ARDS is oftenlimited to patients requiring ventilatory support on the ICU,but less severe forms, conventionally referred to as acutelung injury (ALI) and with similar pathology, occur on acutemedical and surgical wards. The clinical symptoms and


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8.8 COMMON CAUSES OF RESPIRATORY FAILURE IN CRITICALLY ILL PATIENTS

Type 1 respiratory failure

● Pneumonia ● Lung collapse,*● Pulmonary oedema* e.g. retained secretions● Pulmonary embolism ● Asthma● Pulmonary fibrosis ● Pneumothorax● ARDS* ● Pulmonary contusion● Aspiration (blunt chest trauma)

Type 2 respiratory failure

● Reduced respiratory drive,* ● COPDe.g. drug overdose, ● Peripheral neuromuscularhead injury disease, e.g. Guillain–Barré,

● Upper airway obstruction myasthenia gravis(oedema, infection, ● Flail chest injuryforeign body) ● Exhaustion* (includes all

● Late severe acute asthma type 1 causes)

* Secondary complications of other diseases.

Fig. 8.8 Chest X-ray in acute respiratory distress syndrome(ARDS). This 22-year-old woman was involved in a road trafficaccident. Note bilateral lung infiltrates, pneumomediastinum,pneumothoraces with bilateral chest drains, surgical emphysema, andfractures of the ribs, right clavicle and left scapula.

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signs are not specific, sharing many features with otherpulmonary conditions. The criteria defining ARDS are:

● hypoxaemia, defined as PaO2/FIO2 < 26.7 kPa (< 200 mmHg)

● chest X-ray showing diffuse bilateral infiltrates (Fig. 8.8)● absence of a raised left atrial pressure: PAWP < 15 mmHg● impaired lung compliance.

The term ARDS has severe limitations as a diagnosticlabel since, like jaundice or a raised CVP, it represents aresponse to a variety of primary conditions (Box 8.9).

RENAL FAILURE

Oliguria is frequently an early sign of systemic problems in critical illness and successful resuscitation is associatedwith restoration of good urine output, an improving acid–base balance and correction of plasma potassium, urea and creatinine. Acute renal failure (p. 481) in the context ofcritical illness is usually due to pre-renal factors such asuncorrected hypovolaemia, hypotension or ischaemiacausing acute tubular necrosis (ATN). Sepsis is frequently acompounding factor, causing both global hypotension andlocal ischaemia that is often associated with DIC. In thepresence of pre-existing chronic renal impairment ornephrotoxic drugs, acute renal failure may result fromrelatively minor ischaemic or hypotensive insults. WhileATN is by far the most common cause of acute renal failurein the ICU, it is essential not to overlook other causes, such as renal tract obstruction (including a blocked urinarycatheter), drug toxicity, acute glomerulonephritis andvasculitis associated with connective tissue diseases such assystemic lupus erythematosus. Appropriate investigationssuch as urinary microscopy, immunopathological tests andabdominal ultrasound to exclude renal tract obstruction needto be carried out at an early stage.

NEUROLOGICAL FAILURE (COMA)

Impaired consciousness or coma is often an early feature of severe systemic illness (Box 8.10). Prompt assessment of

conscious level and management of airway, breathing andcirculation are essential to prevent further brain injury, toallow diagnosis and for definitive treatment to be instituted.

Impairment of conscious level is objectively gradedaccording to the Glasgow Coma Scale (GCS, p. 1186),which is also used to monitor progress. Although necessarilylimited, careful neurological examination is very importantin the unconscious patient. Pupil size and reaction to light,presence or absence of neck stiffness, focal neurologicalsigns and evidence of other organ impairment should benoted. After cardiorespiratory stability is achieved, the causeof the coma must be sought from history (family, witness,general practitioner), examination and investigation,particularly CT. The possibility of drug overdose shouldalways be considered. The direct neurological causes ofcoma are listed and described in Chapter 26.

SEPSIS

Any or all of the features of SIRS (Box 8.5, p. 185) may bepresent, together with an obvious focus of infection such aspurulent sputum from the chest with shadowing on chest X-ray or erythema around an intravenous line. However,severe sepsis may present as unexplained hypotension (i.e.septic shock) and the speed of onset may simulate a majorpulmonary embolus or myocardial infarction. The commonsites of infection in critically ill patients and some of theappropriate investigations to consider are listed in Box 8.11.

The patient may be admitted with infection from home(‘community-acquired’) or may develop it after admissionto the unit (‘nosocomial’). The likely causative microorgan-ism and the antibiotic sensitivities will depend on thisimportant distinction, which therefore directs the initialchoice of antibiotics. Initial investigations should include:

● cultures of blood, sputum, intravascular lines, urine andany wound discharges

● coagulation profile, plasma lactate, arterial blood gases,urinalysis and chest X-ray.

As few as 10% of ICU patients with a clinical diagnosisof ‘septic’ shock will have positive blood cultures, due to theeffects of prior antibiotic treatment and the fact that a patientwith an inflammatory state is not necessarily infected.

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8.9 CONDITIONS PREDISPOSING TO ARDS

Inhalation (direct)

● Aspiration of gastric contents ● Blunt chest trauma● Toxic gases/burn injury ● Near-drowning● Pneumonia

Blood-borne (indirect)

● Sepsis ● Major blood transfusion● Necrotic tissue reaction

(particularly bowel) ● Anaphylaxis (wasp, bee,● Multiple trauma snake venom)● Pancreatitis ● Fat embolism● Cardiopulmonary bypass ● Carcinomatosis● Severe burns ● Obstetric crises● Drugs (heroin, barbiturates, (amniotic fluid embolus,

thiazides) eclampsia)

8.10 SYSTEMIC CAUSES OF COMA

Cerebral hypoxia; hypercapnia

● Respiratory failure

Cerebral ischaemia

● Cardiac arrest ● Hypotension

Metabolic disturbance

● Diabetes mellitus ● UraemiaHypoglycaemia ● Hepatic failureKetoacidosis ● HypothermiaHyperosmolar coma ● Drugs

● Hyponatraemia ● Sepsis

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Specific investigations will be driven by the history andexamination. For example, erect/decubitus abdominal X-rays, ultrasound and CT might be considered in cases ofsuspected intra-abdominal sepsis (Box 8.11).

The most important objective in management is toidentify and treat the underlying cause. Nosocomialinfections are an increasing problem on critical care units(Box 8.12). Cross-infection is a major concern, particularlywith regard to meticillin-resistant Staphylococcus aureus(MRSA) and multidrug-resistant Gram-negative organisms,and if this is frequent it should prompt a review of the unit’sinfection control policies. The most important practice inpreventing cross-infection is thorough hand-washing afterevery patient contact. Limiting the use of antibiotics helps toprevent the emergence of multidrug-resistant bacteria.

DISSEMINATED INTRAVASCULARCOAGULATION (DIC)

This is also known as consumptive coagulopathy and is one of the acquired disorders of haemostasis (p. 1060); it iscommon in critically ill patients and often heralds the onsetof multi-organ failure. The condition is characterised by anincrease in prothrombin time, partial thromboplastin time

and fibrin degradation products, and a fall in platelets andfibrinogen. The clinically dominant feature may be wide-spread bleeding from vascular access points, gastrointestinaltract, bronchial tree and surgical wound sites, or widespreadmicrovascular and even macrovascular thrombosis.Management is supportive with infusions of fresh frozenplasma and platelets while the underlying cause is treated.

GENERAL PRINCIPLES OF CRITICAL CARE MANAGEMENT

Critically ill patients should be assessed regularly and atleast twice daily on morning and evening ward rounds.Initially, it seems daunting to perform such an assessment,


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8.11 SITES OF INFECTION IN CRITICALLY ILL PATIENTS

Sites of infection Investigations and comments

MAJORIntravenous lines (particularly central) These should always be suspected; if the patient develops evidence of sepsis and the lines have

not been changed for > 4 days, they must be replaced

Lungs The risk of nosocomial pneumonia is high in intubated patients. When the patient has been onthe ICU for > 3–4 days, particularly if antibiotics have been administered, the nasopharynxbecomes colonised with Gram-negative bacteria which migrate to the lower respiratory tract.Prophylaxis using a combination of parenteral and enteral antibiotics (selective decontaminationof the digestive tract) has been shown to reduce incidence of nosocomial pneumonia

Abdomen Intra-abdominal abscesses or necrotic gut must be considered in patients who have hadabdominal surgery. Pancreatitis or acute cholecystitis may develop as a complication of criticalillness. Ultrasound, CT, aspiration of collections of fluid/pus and laparotomy are relevant

Urinary tract A catheter specimen of urine should always be taken in cases of unexplained sepsis but thelower urinary tract is a relatively unusual source of severe sepsis

OTHERHeart valves Transthoracic or transoesophageal echocardiogram

Meninges Lumbar puncture but check coagulation and platelet count first

Joints and bones X-ray, gallium or technetium white cell scan

Nasal sinuses, ears, retropharyngeal space Clinical examination, plain X-ray, CT

Genitourinary tract (particularly post-partum) Per vaginam examination, ultrasound

Gastrointestinal tract Per rectum examination, stool culture, Clostridium difficile toxin, sigmoidoscopy

8.12 RISK FACTORS FOR NOSOCOMIAL INFECTION

● Mechanical ventilation● Trauma● Invasion with catheters—i.v., urinary, nasogastric tubes● Stress ulcer prophylaxis with H2-antagonists● Prolonged length of stay

8.13 THE CRITICALLY ILL OLDER PATIENT

● ICU demography: increasing numbers of critically ill olderpatients are admitted to the ICU; over 50% of patients in manygeneral ICUs are over 65 years old.

● Outcome: affected to some extent by age, as reflected in APACHEII, but age should not be used as the sole criterion for withholdingor withdrawing ICU support.

● Cardiopulmonary resuscitation (CPR): age does affectoutcome. Successful hospital discharge following in-hospital CPRis rare in patients over 70 years old in the presence of significantchronic disease.

● Functional independence: tends to be lost during an ICU stay.● Specific problems:

—Skin fragility and ulceration—Poor muscle strength: difficulty in weaning from ventilator and

in mobilising —Confusion/delirium: compounded by sedatives and analgesics—High prevalence of underlying nutritional deficiency.

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particularly if there is multiple organ failure and no singleunifying diagnosis. A systematic approach is required:

● Receive reports of progress from staff; review specialistopinions and medical/social history.

● Review charts.● Examination: general (rashes, bleeding sites, line sites)

and organ-specific.● Assess information from monitors (check levelling to

reference point, zeroing and calibration, determinewhether they are still required).

● Fluid balance: note previous 24-hour balances, assessintra- and extravascular state of hydration and set targetsfor the bedside nurse for the next 24 hours, specifyingcrystalloid and colloid requirements, the route ofadministration (enteral or parenteral), and volume andfilling pressure limits.

● Nutrition: review calorie intake, route of administration.● Laboratory results: review haematology including

coagulation, biochemistry and bacteriology.● Review antibiotic therapy: note temperature, white

count, line sites etc.● Review drug chart with ICU pharmacist, consider

side-effects and interactions, and identify therapy thatcan be stopped.

● Review X-rays and other specialist investigations.● Make an integrated management plan, specifying goals

for each organ system.

MANAGEMENT OF MAJOR ORGAN FAILURE

CIRCULATORY SUPPORT

The primary goals (Box 8.14) are to:

● Restore global oxygen delivery (DO2) by ensuringadequate cardiac output.

● Maintain an MAP that ensures adequate perfusion of vital

organs. The target will be patient-specific depending onpre-morbid factors (e.g. hypertension or coronary arterydisease) and may range from 60 to 80 mmHg.

● Avoid levels of left atrial pressure that producepulmonary oedema and compromise gas exchange. This may limit the degree of volume resuscitation in the presence of acute lung injury/ARDS.

The first objective is to ensure that an ‘appropriate’ventricular preload is restored. Vasoactive drugs should notbe used as a substitute for adequate volume resuscitation.

The key determinants of DO2 and MAP are cardiac outputand arteriolar resistance which are in turn determined by theventricular ‘preload’, ‘afterload’, myocardial contractilityand heart rate.

PRELOAD

The atrial filling pressures (RAP or CVP, LAP or PAWP) orpreload determine the end-diastolic ventricular volumewhich, according to Starling’s Law and depending on themyocardial contractility, defines the force of the next cardiaccontraction (Fig. 18.21, p. 543). The predominant factorinfluencing preload is venous return, which is determined bythe intravascular volume and the venous ‘tone’ (Box 8.15).

When volume is lost (e.g. major haemorrhage), venous‘tone’ increases and this helps to offset the consequent fallin atrial filling pressure and cardiac output. If the equivalentvolume is returned gradually, the right atrial pressure willreturn to normal as the intravascular volume is restored andthe reflex increase in venous tone abates. However, if fluidis infused too rapidly there will be insufficient time for thevenous and arteriolar tone to fall and pulmonary oedemamay occur, even though the intravascular volume has onlybeen restored to the pre-morbid level.

If the preload is low, volume loading with intravenousfluids is the priority and the most appropriate means of improving cardiac output and oxygen delivery. Thechoice of fluid for volume loading is controversial. No clearadvantage of colloid over crystalloid has ever beendemonstrated, but adequate filling is achieved with smallervolumes of colloid. Red cells have traditionally beentransfused to achieve and maintain an Hb concentration of100 g/l but, in the absence of significant heart disease, atarget of 70–90 g/l may be preferable (Box 24.19, p. 1019).Fluid challenges of 200–250 ml should be titrated againstCVP measurements (Fig. 8.1, p. 180).

When the preload is high, due to excessive intravascularvolume or impaired myocardial contractility, it is advisableto remove volume from the circulation (diuretics, vene-section, haemofiltration) or increase the capacity of thevascular bed using venodilator therapy (glyceryl trinitrate,morphine).

M A N A G E M E N T O F M A J O R O R G A N F A I L U R E

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8.14 INITIAL MANAGEMENT OF CIRCULATORY COLLAPSE

● Monitor MAP, CVP● Correct hypoxaemia● Correct hypovolaemia

If CVP < +6 mmHg from mid-axillary line give volumechallenge (250 ml normal saline or colloid)If CVP > +6 mmHg or poor ventricular function is suspected,use only 100 ml of fluid and consider insertion of PA catheterto direct further treatment with fluids and vasoactive agents

● Achieve target MAP (using vasoactive agents only afterhypovolaemia corrected)

● Monitor trend in arterial blood gases, pH, base deficit and lactate● Consider intubation if

PaCO2 > 6.5 kPa (> 50 mmHg)Respiratory rate > 25/minImpaired consciousness: GCS ≤ 7

● Correct acidaemia with i.v. bicarbonate if H+ > 63 nmol/l (pH < 7.20) and PaCO2 < 6 kPa (< 45 mmHg) (i.e. base excess > –10 mmol/l)

8.15 FACTORS INFLUENCING CENTRAL VENOUS PRESSURE

● Intravascular volume● Venous tone● Right heart function and ‘afterload’, i.e. PAP● Intrathoracic pressure

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AFTERLOAD

The tension in the ventricular myocardium during systole, or ‘afterload’, is determined by the resistance to ventricularoutflow, which is a function of the peripheral arteriolarresistance. If the considerable assumption is made that flowin the circulation is linear and non-pulsatile, the resistanceagainst which each ventricle works may be calculated as thepressure drop across the resistance bed divided by the flow:

Systemic vascular resistance (SVR) = (MAP – RAP)/QT

Pulmonary vascular resistance (PVR) = (PAP − LAP)/QT

If the pressures are measured in mmHg and flow inlitres/min, these calculations give the resistances in simpleor ‘Wood’ units; multiplication by 80 converts to SI units.For a normal 70 kg adult:

SVR = (90 − 0)/5 × 80 = 1440 dyn.sec/cm5

PVR = (10 − 5)/5 × 80 = 80 dyn.sec/cm5

Understanding the reciprocal relationship betweenpressure, flow and resistance is crucial for appropriatecirculatory management. High resistances produce lowerflows at higher pressures for a given amount of ventricularwork. Therefore, a systemic vasodilator such as sodiumnitroprusside will allow the same cardiac output to bemaintained for less ventricular work but with a reducedarterial blood pressure. In hyperdynamic sepsis, the SVRand blood pressure are low but the cardiac output is high;therefore a vasoconstrictor (noradrenaline (norepinephrine),vasopressin) is appropriate to restore BP, albeit with somereduction in cardiac output.

MYOCARDIAL CONTRACTILITY

This determines the work that the ventricle performs undergiven loading conditions or, put another way, the stroke

volume that the ventricle will generate against a givenafterload for a particular level of preload.

The relationship between stroke work and filling pressureis shown in Figure 18.21, page 543. The ventricular strokework is the external work performed by the ventricle witheach beat and is calculated from the stroke volume (SV) andthe pre- and afterload pressures:

Ventricular stroke work (VSW) = SV × (afterload − preload)

e.g. LVSW = SV × (MAP − LAP) ml.mmHg

Using the data for a normal adult shown in Box 8.6 (p. 186) and multiplying by 0.0136 to convert to SI units of gram.metres, LVSW and RVSW are 80 and 10 g.mrespectively.

Consideration of ventricular work is important because it is desirable to maintain satisfactory perfusion and oxygendelivery to all organs at maximum cardiac efficiency andtherefore minimise myocardial ischaemia. Myocardialcontractility is frequently reduced in critically ill patients dueto either pre-existing cardiac disease (usually ischaemic heartdisease) or the disease process itself (particularly sepsis).

THERAPEUTIC OPTIONS IN THEMANAGEMENT OF CARDIAC FAILURE

If the cardiac output is inadequate and myocardial contract-ility is poor, the available treatment options are to:

● Reduce afterload. This can be achieved by using anarteriolar dilator (e.g. nitrates, ACE inhibitor), whichmay be limited by the consequent fall in systemicpressure. A counterpulsation balloon pump offers theideal physiological treatment because it reduces LVafterload while increasing cardiac output, diastolicpressure and coronary perfusion; it is particularlyvaluable in treating myocardial ischaemia.


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8.16 CIRCULATORY EFFECTS OF COMMONLY USED VASOACTIVE DRUG INFUSIONS

Cardiac Heart Blood Cardiac Splanchnic Drug (receptors) contractility rate pressure output blood flow SVR PVR

Dopamine(< 5 μg/kg/min) (DA1,b1,a) ↑ →/↑ →/↑ ↑ →/↑ →/↑ →/↑(> 5 μg/kg/min) ) (b1,a,DA1,b2) ↑↑ ↑ ↑ ↑↑ → ↑ ↑Adrenaline (epinephrine) (b1,a,b2) ↑↑ ↑ ↑↑ ↑↑↑ ↓ ↑ ↑Noradrenaline (norepinephrine) (a,b1) →/↑ →/↓ ↑↑ →/↓ →/↓ ↑↑ ↑↑Isoprenaline (b1,b2) ↑ ↑↑ →/↓ ↑ →/↑ →/↓ ↓Dobutamine (b1,b2,a) ↑ ↑ →/↓ ↑↑ → ↓ ↓Dopexamine (b2, DA1, DA2) ↑ ↑↑ →/↓ ↑ ↑ ↓ ↓Glyceryl trinitrate (NO) → ↑ ↓ ↑ ↑ ↓ ↓Nitroprusside (NO) → ↑ ↓ ↑ ↑ ↓ ↓Epoprostenol (prostacyclin) → ↑ ↓ ↑ ↑ ↓ ↓Milrinone (PDEI) →/↑ ↑ ↓ ↑↑ ↑ ↓ ↓

Receptors through which these vasoactive drugs work are given in parentheses and listed in order of the extent of receptor stimulation produced.Note that dopamine acts more like adrenaline at high doses. (α = α-adrenoceptor; β1, β2 = β-adrenoceptors 1 and 2; DA1, DA2 = dopaminergicreceptors 1 and 2; NO = acts via local nitric oxide release; PDEI = phosphodiesterase inhibitor.)

The global circulatory effects listed are guidelines only. The magnitude of the response will depend on the circulatory state of the patient whenthe drug is started, the dose of the drug administered and the receptor distribution and density in specific vascular beds.

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● Increase preload. However, if there is significantimpairment of myocardial contractility, givingintravascular volume to increase filling pressures willonly produce a small increase in stroke volume andcardiac output and risks precipitating pulmonary oedema.

● Improve myocardial contractility. Box 8.16. lists somecharacteristics of the commonly used inotropic agents.

● Control heart rate and rhythm (pp. 560–575). Theoptimum heart rate is usually between 90 and 110 perminute. Correction of low serum potassium andmagnesium concentrations should be the first stage intreating tachyarrhythmias in the critically ill. Atrialfibrillation is particularly common and troublesome in septic and critically ill patients; amiodarone 300 mgover 30–60 minutes, followed by 900 mg over 24 hours, can be successful in controlling ventricularrate and in restoring and maintaining sinus rhythm.

The management of tamponade and pulmonary embolismis described on pages 645 and 724 respectively and specificaspects of management in sepsis are described later (p. 199).

RESPIRATORY SUPPORT

Respiratory support is indicated to maintain the patency ofthe airway, correct hypoxaemia and hypercapnia, and reducethe work of breathing. It ranges from oxygen therapy byfacemask, through non-invasive techniques such as CPAP(Box 8.17) and non-invasive positive pressure ventilation(NIPPV), to full ventilation via an endotracheal tube ortracheostomy.

OXYGEN THERAPY

Oxygen is given to treat hypoxaemia and ensure adequatearterial oxygenation (SpO2 > 90%). It should initially begiven by facemask or nasal cannulae and the inspiredoxygen concentration (FIO2) can then be adjusted accordingto the results of pulse oximetry and arterial blood gasanalysis. The risk of progressive hypercapnia in certainpatients with COPD who are dependent on hypoxic drivehas been overstated. If administration of oxygen to ensureSpO2 > 90% results in unacceptable hypercapnia, the patientalmost certainly requires some form of mechanicalrespiratory support. The theoretical risks of oxygen toxicityare not relevant if the patient is acutely hypoxaemic. It isvital to maintain cerebral oxygenation even at the risk of pulmonary toxicity because hypoxic cerebral damage is irreversible. More detail on oxygen therapy is given onpage 668.

NON-INVASIVE RESPIRATORY SUPPORT

If a patient remains hypoxaemic on high-flow oxygen, other measures are required to improve oxygenation and toreduce the work of breathing. If the patient has respiratoryfailure associated with decreased lung volume, applicationof continuous positive airways pressure (CPAP, Box 8.17)will both improve oxygenation by recruitment of under-ventilated alveoli, and reduce the work of breathing by


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8.17 MODES AND TERMS USED IN MECHANICAL VENTILATORY SUPPORT

Intermittent positive pressure ventilation (IPPV)

● Generic term for all types of positive pressure ventilation

Controlled mandatory ventilation (CMV)

● Most basic classic form of ventilation● Pre-set rate and tidal volume● Does not allow spontaneous breaths● Appropriate for initial control of patients with little respiratory

drive, severe lung injury or circulatory instability

Synchronised intermittent mandatory ventilation (SIMV)

● Pre-set rate of mandatory breaths with pre-set tidal volume

● Allows spontaneous breaths between mandatory breaths● Spontaneous breaths may be pressure-supported (PS)● Allows patient to settle on ventilator with less sedation

Pressure controlled ventilation (PCV)

● Pre-set rate; pre-set inspiratory pressure● Tidal volume depends on pre-set pressure, lung compliance and

airways resistance● Used in management of severe acute respiratory failure to avoid

high airway pressure, often with prolonged inspiratory to expiratory ratio (pressure controlled inverse ratio ventilation,PCIRV)

Pressure support ventilation (PSV)

● Breaths are triggered by patient● Provides positive pressure to augment patient’s breaths● Useful for weaning● Usually combined with CPAP; may be combined with SIMV ● Pressure support is titrated against tidal volume and respiratory

rate

Positive end-expiratory pressure (PEEP)

● Positive airway pressure applied during expiratory phase in patients receiving mechanical ventilation

● Improves oxygenation by recruiting atelectatic or oedematous lung

● May impair venous return and reduce cardiac output

Continuous positive airways pressure (CPAP)

● Positive airway pressure applied throughout the respiratory cycle, via either an endotracheal tube or a tight-fitting facemask

● Fresh gas flow must exceed patient’s peak inspiratory flow

● Improves oxygenation by recruitment of atelectatic or oedematous lung

● Mask CPAP discourages coughing and clearance of lung secretions; may increase the risk of aspiration

Bi-level positive airway pressure (BiPAP/BIPAP)

● Describes situation of two levels of positive airway pressure (higher level in inspiration)

● In fully ventilated patients, BiPAP is essentially the same as PCV with PEEP

● In partially ventilated patients, and especially if used non-invasively, BiPAP is essentially PSV with CPAP

Non-invasive intermittent positive pressure ventilation (NIPPV)

● Most modes of ventilation may be applied via a facemask or nasal mask

● Usually PSV/BiPAP (typically 15–20 cmH2O) often with back-up mandatory rate

● Indications include acute exacerbations of COPD

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improving lung compliance. CPAP is most successful inclinical situations where alveoli are readily recruited, suchas in pulmonary oedema and post-operative collapse/atelectasis. It is also helpful in treating pneumonia,especially in immunocompromised patients. The risk ofnosocomial infection is reduced by avoiding endotrachealintubation. A CPAP mask often becomes uncomfortable andgastric distension may occur. Patients must therefore becooperative, be able to protect their airway and have thestrength to breathe spontaneously and cough effectively.

NIPPV refers to ventilatory support by nasal or fullfacemask. It may avoid the need for endotracheal intubationin patients with type 2 respiratory failure, typically thosewith exacerbations of COPD, and it may be used duringweaning from conventional ventilation. As with mask CPAP,NIPPV requires the patient to be conscious and cooperative.

ENDOTRACHEAL INTUBATION ANDMECHANICAL VENTILATION

Over 60% of patients appropriately admitted to ICU requireendotracheal intubation and mechanical ventilation, mostlyfor respiratory failure but also for other reasons (Boxes 8.18and 8.19).

The final decision to perform tracheal intubation andventilate a patient should be taken on clinical grounds ratherthan as a response to the results of particular investigations.

In the conscious patient, intubation requires induction ofanaesthesia and muscle relaxation, while in more obtundedpatients sedation alone may be adequate. This can behazardous in the critically ill patient with respiratory andoften cardiovascular failure. Continuous monitoring,particularly of heart rate and BP (preferably invasively), is essential, and resuscitation drugs must be immediatelyavailable. Hypotension commonly follows sedation oranaesthesia because of direct cardiovascular effects of thedrugs and loss of sympathetic drive; positive pressureventilation may compound this problem by increasing intra-thoracic pressure, thereby reducing venous return and hencecardiac output.

The different types of ventilatory support are illustrated in Figure 8.9. Modern ventilators allow considerableflexibility in the level of support from controlled mandatoryventilation to partial ventilatory support modes, and assistedspontaneous breathing which allows the ventilator torespond to patients’ demands. Use of partial ventilatorysupport avoids the requirement for and hazards of paralysisand deep sedation, and allows the patient to be consciousand yet comfortable.


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8.18 CLINICAL CONDITIONS REQUIRING MECHANICAL VENTILATION*

Post-operative● e.g. After major abdominal or cardiac surgery

Respiratory failure● ARDS ● Acute severe asthma● Pneumonia ● Aspiration● COPD ● Smoke inhalation, burns

Circulatory failure● Following cardiac arrest ● Low cardiac output—● Pulmonary oedema cardiogenic shock

Neurological disease● Coma of any cause● Status epilepticus● Drug overdose● Respiratory muscle failure (e.g. Guillain–Barré, poliomyelitis,

myasthenia gravis)● Head injury—to avoid hypoxaemia and hypercapnia, and to

reduce intracranial pressure● Bulbar abnormalities causing risk of aspiration (e.g.

cerebrovascular accident, myasthenia gravis)

Multiple trauma

*Additional considerations:Metabolic rate (ventilatory requirements rise as metabolic rate increases) Nutritional reserve (low potassium or phosphate reduces respiratory muscle power)Condition of the abdomen (distension due to surgery or tenseascites causes both discomfort and splinting of the diaphragm,compromising spontaneous respiratory effort and promotingbilateral basal lung collapse)

8.19 INDICATIONS FOR TRACHEAL INTUBATION ANDMECHANICAL VENTILATION

● Protection of airway● Removal of secretions● Hypoxaemia (PaO2 < 8 kPa (< 60 mmHg); SpO2 < 90%) despite

CPAP with F IO2 > 0.6● Hypercapnia if conscious level impaired or risk of raised

intracranial pressure● Vital capacity falling below 1.2 litres in patients with

neuromuscular disease● Removing the work of breathing in exhausted patients

Mechanical ventilation

Non-invasive

IPPV -ve pressure

Partialsupport

Fullsupport

CPAPBiPAPNIPPV

CuirassTank: 'iron lung'

Rocking bed

SIMVPSV

BiPAP

CMV

Volumecontrol

Pressurecontrol

Invasive(via ET or

tracheostomy tube)

+ve pressure(via face ornasal mask)

Fig. 8.9 Different types of invasive and non-invasive ventilatorysupport. (ET = endotracheal; see Box 8.17 for other abbreviations.)

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General considerations in the managementof the ventilated/intubated patient● Beware of the restless patient. Try to establish the cause

of the problem before simply administering sedation.Possibilities include pneumothorax, hypoxaemia,hypercapnia due to inadequate ventilation, pain, onset ofsepsis, cardiac decompensation (pulmonary oedema,dysrhythmia, infarction) and proximal airwayobstruction, e.g. secretions.

● Patients who are breathing spontaneously adjust theirventilation to compensate for metabolic derangements;this cannot occur in patients who are ventilated usingmandatory modes so the clinician must either correct theunderlying metabolic abnormality or make appropriatechanges to the ventilator settings. For example, a patientwith severe diabetic ketoacidosis will hyperventilate tocompensate for the metabolic acidosis; if mechanicalventilation is instituted, there will be a potentiallycatastrophic fall in pH unless the acidosis is corrected byadministering sodium bicarbonate or a high minutevolume (artificial hyperventilation) is delivered.

● Ventilator should be set to detect:— minimum acceptable minute volume to identify

inadvertent disconnection— maximum acceptable airway pressure to prevent

barotrauma.● Humidify and warm inspired gas to prevent inspissation

of secretions.● Arrange regular positioning, physiotherapy and suctioning

to clear secretions and prevent proximal airwayobstruction and distal alveolar collapse. The patientshould be in a 30° head-up position to avoid aspiration.

● Obtain a chest X-ray to check the position of theendotracheal tube following intubation (the appropriateposition is 4 cm above the carina).

● Bronchoscopy should be readily available to:— investigate upper airways obstruction (plugging of

the proximal bronchial tree by inspissated mucus isthe most common cause)

— investigate lobar/segmental collapse, and aspiratemucus plug obstructing proximal bronchial tree

— assist in cases of difficult intubation or tracheostomytube change

— obtain bronchoalveolar lavage specimens formicrobiology

— identify the cause of haemoptysis (not always easy)— exclude tracheobronchial disruption after thoracic

trauma.

Ventilation strategyThe selection of ventilator mode and settings for tidalvolume, respiratory rate, positive end-expiratory pressure(PEEP) and inspiratory to expiratory ratio is dependent onthe cause of the respiratory failure. The objectives are to:

● improve gas exchange● minimise damage to the lung by avoiding high lung

volumes and F IO2

● avoid adverse circulatory effects● make the patient comfortable without heavy sedation or

muscle paralysis by reducing the work of breathing andharmonising interaction between patient and ventilator.

In asthma and conditions with increased lung volumes(high FRC) a prolonged expiratory phase is necessary toprevent progressive lung over-inflation; PEEP and largetidal volumes exacerbate over-distension, produce highalveolar pressures and increase the risk of pneumothorax.High intrathoracic pressures compromise circulatoryfunction, particularly if there is intravascular volumedepletion, so that oxygen delivery may actually fall in spiteof improved arterial oxygenation.

In patients with alveolar collapse (low FRC), such asthose with ARDS, it is appropriate to use a prolongedinspiratory to expiratory ratio and high levels of PEEP (+10to +15 cmH2O) to recruit alveoli and improve complianceand gas exchange (Boxes 8.20 and 8.21). Recent studieshave shown that in ARDS, damage to the lungs can beexacerbated by mechanical ventilation, possibly by over-distension of alveoli and repeated opening and closure ofdistal airways.

Other management strategies which may be of benefit insevere ARDS include prone ventilation, nitric oxideinhalation and corticosteroids.

Prone ventilationProne positioning improves oxygenation significantly intwo-thirds of patients with ARDS by reducing thoraco-abdominal compliance and the vertical pleural pressuregradient so that ventilation is more evenly distributed andbetter matched to perfusion. Multicentre trials using manualpronation have failed to show a survival benefit and trialsusing an automatic rotating bed are underway.


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8.20 PRINCIPLES OF MECHANICAL VENTILATION IN ARDS

● Optimum ventilator settings are:Pressure-controlledLong inspiratory to expiratory time Positive end-expiratory pressure (PEEP)

● Allow PaCO2 to rise (permissive hypercapnia) and tolerate loweroxygen saturations than normal (e.g. 88–90%)

● Avoid:Large tidal volumes (ideally 6 ml/kg) Airway pressure of more than 35 cmH2OF IO2 of more than 0.8 if possible

● Remember that high intrathoracic pressures compromisecirculatory function so oxygen delivery may actually fall in spiteof improved oxygenation

● Management must be a balance between improving gasexchange, minimising the risk of subsequent pulmonary fibrosisdue to lung injury, and avoiding adverse circulatory effects

8.21 OPTIMAL VENTILATION IN ARDS

‘Ventilation using positive end-expiratory pressure but limiting tidalvolumes to 5–7 ml/kg and accepting high PaCO2 levels improvesoutcome in ARDS.’● Amato MB, et al. N Engl J Med 1998; 338:347–354.● Acute Respiratory Distress Syndrome Network. N Engl J Med 2000; 342:1301–1308.

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Inhaled nitric oxideNitric oxide is a very short-acting pulmonary vasodilator.Delivered to the airway in concentrations of between 1 and20 parts per million, it improves blood flow to ventilatedalveoli, thus improving ventilation–perfusion matching.Oxygenation can be improved markedly in some patientsbut the evidence indicates that the benefit only lasts for 48hours and outcome is not improved.

Pharmacological therapyThere is now considerable evidence that corticosteroidsimprove outcome if given in the fibroproliferative stage ofARDS. A trial of corticosteroids is therefore indicated if apatient with ARDS has consistent gas exchange impairment and ventilator dependence at 7–10 days after diagnosis. Therecommended dose of methylprednisolone is 2–3 mg/kg/day, decreasing after 7 days and as gas exchange improves.Bronchoscopy and bronchoalveolar lavage should beperformed to identify or exclude pulmonary infection beforecommencing corticosteroid therapy.

Weaning from respiratory supportThis is the process of progressively reducing and eventuallyremoving all external ventilatory support and associatedapparatus. The majority of patients require mechanicalventilatory support for only a few days and do not needweaning. In these patients simple trials of spontaneousbreathing via the endotracheal tube will usually indicatewhether the patient can be successfully extubated or not.

In contrast, patients who have required long-termventilatory support for severe lung disease, e.g. ARDS, mayinitially be unable to sustain even a modest degree of respi-ratory work because of residual decreased lung complianceand hence increased work of breathing, compounded byrespiratory muscle weakness. These patients thereforerequire weaning until respiratory muscle strength improvesto the point that all support can be discontinued.

Weaning techniques involve the patient breathingspontaneously for increasing periods of the day and agradual reduction in the level of ventilatory support. Thisoften involves graduation to partial support modes and thennon-invasive modes of ventilatory support.

Increasingly, the process of identifying patients able toprogress to spontaneous breathing and extubation is doneaccording to a ‘weaning protocol’. This entails decidingwhether a patient can be safely subjected to a spontaneousbreathing trial (Box 8.22). If the patient meets the criteria

listed, he or she undergoes the breathing trial for 2–5 minutes.The respiratory rate and tidal volume are noted, and the ratiocalculated. If it is less than 105 breaths/min/litre, the patientcontinues the trial for a further 30 minutes to 2 hours periodbefore extubation.

In the event of failure (increased respiratory rate;decreased tidal volume) gradual weaning of ventilationcontinues using synchronised intermittent mandatoryventilation (SIMV), pressure support ventilation (PSV) orintermittent periods of spontaneous breathing. Non-invasiveventilation via a facemask can allow earlier extubation incertain groups of patients, e.g. chronic obstructive pulmo-nary disease, with weaning continuing after removal of theendotracheal tube.

Despite the development of a number of objective testsand indices of the patient’s ability to sustain spontaneousventilation, the decision to extubate and the speed ofweaning from mechanical ventilation still rely largely onclinical judgement.

TracheostomyTracheostomy is usually performed electively whenendotracheal intubation is likely to be prolonged (over 14days). Tracheostomies have benefits in terms of patientcomfort, aid weaning from ventilation (since sedation can bereduced or stopped), and allow access for tracheal toilet andintermittent respiratory support (Box 8.23).

Tracheostomy is now usually carried out using apercutaneous technique in the ICU, which avoids the needfor transfer to the operating theatre. This has led to earlierand more frequent use of tracheostomy. Preliminaryevidence indicates that early tracheostomy (at < 3 days) inpatients predicted to require prolonged ventilation leads to areduced length of ICU stay, and decreased morbidity andmortality.

Mini-tracheostomyThe passage of a smaller (4.5 mm internal diameter) tubethrough the cricothyroid membrane is a useful technique toclear airway secretions in spontaneously breathing patientswith a poor cough effort. It can be particularly useful in theHDU and in post-operative patients.


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8.22 FACTORS IN DECIDING WHETHER A VENTILATED PATIENT CAN BE WEANED AND SAFELY EXTUBATED

● Has the original indication for mechanical ventilation resolved?● Is the patient conscious and able to cough and protect his/her

airway?● Is the circulation stable, with a normal or reasonably low left

atrial pressure?● Is gas exchange satisfactory (PO2 > 8 kPa (> 60 mmHg) on

F IO2 < 0.5; PCO2 < 6 kPa (< 45 mmHg))?● Is analgesia adequate?● Are any metabolic problems well controlled?

8.23 ADVANTAGES AND DISADVANTAGES OF TRACHEOSTOMY

Advantages

● Patient comfort● Improved oral hygiene● Reduced sedation requirement● Enables speech with cuff deflated and a speaking valve attached● Earlier weaning and ICU discharge● Access for tracheal toilet● Reduces vocal cord damage

Disadvantages

● Immediate complications: hypoxia, haemorrhage● Tracheal damage; late stenosis● Tracheostomy site infection

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RENAL SUPPORT

Oliguria (< 0.5 ml/kg/hr for 2–3 hours) requires explanationand early intervention to correct hypoxaemia, hypo-volaemia, hypotension and renal hypoperfusion. There islittle evidence that specific treatments aimed at inducing adiuresis, such as low-dose dopamine, furosemide ormannitol, have renoprotective action or additional beneficialvalue in restoring renal function beyond aggressivehaemodynamic resuscitation to achieve normovolaemia,normotension and an appropriate cardiac output. Sepsis isfrequently implicated in the development of acute renalfailure and the focus must be promptly and adequatelytreated by surgical drainage and antibiotics if renal functionis to be restored. Obstruction of the renal tract should alwaysbe excluded by abdominal ultrasound and, if present, shouldbe relieved.

If renal function cannot be restored following resus-citation, renal replacement therapy (p. 491) is indicated(Box 8.24).

The preferred renal replacement therapy in ICU patientsis pumped venovenous haemofiltration. This is associatedwith fewer osmotic fluid shifts and hence greaterhaemodynamic stability than haemodialysis. It is carried outusing a double-lumen central venous catheter placedpercutaneously. Haemofiltration should be continuous;higher rates of filtration (preferably > 35 ml/kg/hr) areassociated with improved outcome. Intermittent treatmentshould only be used when the patient is recovering from the primary insult and return of normal renal function isexpected. Provided the precipitating cause can be success-fully treated, renal failure due to ATN usually recoversbetween 5 days and several weeks later.

Survival rates from multiple organ failure including acuterenal failure have been around 50% for many years butrecent evidence suggests that modern haemofiltrationtechniques are producing better outcomes.

GASTROINTESTINAL AND HEPATICSUPPORT

The gastrointestinal tract and liver play an important role in the evolution of multiple organ failure, even when theprimary diagnosis is not related to the abdomen. Gastro-intestinal symptoms such as nausea, vomiting and large

nasogastric aspirates may be the earliest signs of regionalcirculatory failure and, when associated with a tender,distended, silent abdomen, indicate the probable site of theprimary pathology. Ischaemic bowel is difficult to diagnosein the critically ill patient but, in the context of an otherwiseunexplained lactic acidosis, hyperkalaemia and coagulo-pathy, urgent laparotomy must be considered (p. 922).

The gut has a very rapid cell turnover rate and fastingalone can produce marked changes in mucosal structure and function. In hypovolaemic and frank shock states,splanchnic vasoconstriction produces gut mucosal ischae-mia, damaging the mucosal barrier and allowing toxins toenter the portal circulation and lymphatics. Althoughequipped to cope with moderate portal toxaemia, the livermay be overwhelmed and will then augment the inflamma-tory response itself by releasing cytokines into the systemiccirculation. For this reason the gut has been described as the‘undrained abscess’ or ‘motor’ of multiple organ failure.

Manifestations of MOF within the gastrointestinal tractinclude erosive gastritis, stress ulceration, bleeding,ischaemia, pancreatitis and acalculous cholecystitis.Adequacy of gastric mucosal perfusion can be assessed by gastric tonometry, a technique that uses a modified naso-gastric tube with a balloon containing either saline or air tomeasure intramucosal pH (pHi) or PCO2i. An increaseddifference between gastric PCO2 and arterial PCO2 or anintramucosal acidosis (pHi < 7.32) implies mucosalischaemia.

Early institution of enteral nutrition is the most effectivestrategy for protecting the gut mucosa and providingnutritional support. There is evidence suggesting thatnasogastric feeds supplemented with arginine, omega 3 fattyacids and nucleotides (‘immunonutrition’) may improveoutcome in critical illness. Glutamine supplementation is logical, although not of proven benefit, since it is a‘conditionally essential’ amino acid and the principal energysubstrate used by the gut mucosa in critical illness. Totalparenteral nutrition (TPN) should only be started if allattempts at implementing enteral feeding, includingnasojejunal delivery, have failed; it should be necessary infewer than 10% of general ICU patients.

Recent evidence from a randomised controlled trial(RCT) demonstrates improved outcomes in the critically illresulting from tight glycaemic control (Box 8.25). Manypatients in ICU will require insulin to maintain a bloodsugar between 4.5 and 6.5 mmol/l (~ 80–120 mg/dl), whenon either enteral or parenteral feeding.

Ranitidine and sucralfate are both used to reduce the riskof gastrointestinal haemorrhage, although ranitidine is themore effective. Both agents are associated with an increased


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8.24 INDICATIONS FOR RENAL REPLACEMENT THERAPY

● Fluid overload; pulmonary oedema● Hyperkalaemia: potassium > 6 mmol/l despite medical

management● Metabolic acidosis: H+ > 56 nmol/l (pH < 7.25)● Uraemia:

Urea > 30–35 mmol/l (180–210 mg/dl)Creatinine > 600 μmol/l (> 6.78 mg/dl)

● Drug removal, in overdose situations● Sepsis: tentative evidence for mediator removal

8.25 INTENSIVE INSULIN THERAPY IN CRITICALLY ILL PATIENTS

‘Intensive insulin therapy to maintain blood glucose at or below 6.1 mmol/l (110 mg/dl) substantially reduces morbidity andmortality among critically ill patients in a surgical intensive care unit(34% reduction in in-hospital mortality).’● Van den Berghe G, et al. N Engl J Med 2001; 345:1359–1367

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incidence of nosocomial pneumonia. Treatment should bestopped when full enteral nutrition has been established andis probably only necessary in patients with a history ofpeptic ulcer and those who have evidence of MOF, andparticularly severe coagulopathy.

The hepatic circulation, 80% of which is derived from the portal venous system, is compromised by the samefactors which lead to splanchnic vasoconstriction. Hepaticischaemia leads to impaired filtering of endotoxin from theportal circulation and, as SIRS develops, inflammatorymediators (e.g. cytokines IL-1, IL-6 and TNF) are releasedfrom activated Kupffer cells (hepatic macrophages) into the systemic circulation, increasing the risk of acute renalfailure and the other manifestations of MOF developing.Increased metabolic activity in the liver as a result of sepsis and the need for vasoconstricting agents to maintainblood pressure increase hepatic ischaemia. The syntheticinodilator dopexamine with dopaminergic 1 and 2 and β-adrenergic effects may enhance splanchnic blood flow buthas not been shown to improve outcome.

Two distinctive hepatic dysfunction syndromes occur inthe critically ill:

● Shock liver or ischaemic hepatitis results from extremehepatic tissue hypoxia and is characterised bycentrilobular hepatocellular necrosis. Transaminaselevels are often massively raised (> 1000–5000 U/l) at an early stage, followed by moderatehyperbilirubinaemia (< 100 μmol/l, < 5.8 mg/dl). Thereis often associated hypoglycaemia, coagulopathy andlactic acidosis. Following successful resuscitation,hepatic function generally returns to normal.

● Hyperbilirubinaemia (‘ICU jaundice’) frequentlydevelops following trauma or sepsis, particularly if thereis inadequate control of the inflammatory process. Thereis a marked rise in bilirubin levels (predominantlyconjugated) but only mild elevation of transaminase andalkaline phosphatase levels. This results from failure ofbilirubin transport within the liver and produces thehistological appearance of intrahepatic cholestasis.Extrahepatic cholestasis must be excluded by abdominalultrasound and potentially hepatotoxic drugs should bestopped. Treatment is non-specific and should includeearly institution of enteral feeding. Therapy thatcompromises splanchnic blood flow, particularly highdoses of vasoconstrictor agents, should be avoided.

NEUROLOGICAL SUPPORT

A diverse range of primary neurological and metabolicconditions require management in the ICU. These includethe various causes of coma, spinal cord injury, peripheralneuromuscular disease and prolonged seizures. Intensivecare is required to:

● manage acute brain injury with control of raisedintracranial pressure

● protect the airway, if necessary by endotracheal intubation● provide respiratory support to correct hypoxaemia and

hypercapnia

● treat circulatory problems, e.g. neurogenic pulmonaryoedema in subarachnoid haemorrhage, autonomicdisturbances in Guillain–Barré syndrome, spinal shockfollowing high spinal cord injuries

● manage status epilepticus using anaesthetic agents suchas thiopental or propofol.

The aim of management in acute brain injury is tooptimise cerebral oxygen delivery by maintaining a normalarterial oxygen content and a cerebral perfusion pressureabove 70 mmHg. Avoiding secondary insults to the brainsuch as hypoxaemia and hypotension improves outcome inhead injury. Intracranial pressure (ICP) rises in acute braininjury as a result of haematoma, contusions or ischaemicswelling. Raised ICP is damaging both directly to thecerebral cortex and by producing downward pressure on thebrain stem, and indirectly by reducing cerebral perfusionpressure, thereby threatening cerebral blood flow andoxygen delivery:

Cerebral perfusion pressure (CPP) = mean BP − ICP

ICP may be measured via pressure transducers inserteddirectly into the brain tissue or held in place on the dura. Thenormal upper limit for ICP is 15 mmHg and managementshould be directed at keeping ICP below 20 mmHg (Box8.26). Sustained pressures above 30 mmHg are associatedwith a poor prognosis.

Cerebral perfusion pressure should be maintained above70 mmHg by ensuring adequate fluid replacement and ifnecessary by treating hypotension with a vasopressor suchas noradrenaline (norepinephrine).

Complex neurological monitoring must be combined withfrequent clinical assessment, i.e. GCS, pupil response tolight and focal neurological signs. The motor response topain is a particularly important prognostic sign. No responseor extension of the upper limbs is associated with severeinjury, and unless there is improvement within a few daysprognosis is very poor. A flexor response is encouraging andindicates that a good outcome is still possible.


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8.26 STRATEGIES TO CONTROL INTRACRANIAL PRESSURE

● Sedation, analgesia and occasionally paralysis to preventcoughing

● Nurse with 30° head-up tilt and avoid excessive flexion of thehead or pressure around the neck that may impair cerebralvenous drainage

● Control epileptiform activity with appropriate anticonvulsanttherapy; an electroencephalogram (EEG) may be necessary toensure this is achieved

● Maintain strict glycaemic control with blood glucose between 4 and 8 mmol/l (~ 70–140 mg/dl)

● Aim for a core body temperature of between 36 and 37°C● Maintain sodium > 140 mmol/l using i.v. normal saline● Avoid dehydration or fluid overload● Hyperventilation to reduce the PCO2 to 4–4.5 kPa

(~ 30–34 mmHg) for the first 24 hours● Osmotic diuretic, mannitol 20% 100–200 ml (0.25–0.5 g/kg),

coupled with volume replacement● Hypnotic infusion, thiopental, titrated to ‘burst suppression’

on EEG● Surgery: drainage of haematoma or ventricles; lobectomy,

decompressive craniectomy

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NEUROLOGICAL COMPLICATIONS ININTENSIVE CARE

Neurological complications also occur as a result ofsystemic critical illness. Sepsis may be associated with anencephalopathy characterised by confusion/delirium andassociated with cerebral oedema and loss of vasoregulation.Hypotension and coagulopathy may provoke cerebralinfarction or haemorrhage. Neurological examination isvery difficult if the patient is sedated or paralysed and it isimportant to stop sedation regularly to reassess the patient’sunderlying level of consciousness. If there is evidence of afocal neurological deficit or a markedly declining level ofconsciousness, a CT of the brain should be performed.

Critical illness polyneuropathy is another potentialcomplication in patients with sepsis and MOF. It is due toperipheral nerve axonal loss rather than demyelination andcan result in areflexia, gross muscle-wasting and failure towean from the ventilator, thus prolonging the duration ofintensive care. Recovery can take many weeks.

MANAGEMENT OF SEPSIS

Prompt administration of appropriate antibiotics with aspectrum wide enough to cover probable causative organ-isms, based on an analysis of the likely site of infection,previous antibiotic therapy and the known resistancepatterns on the unit, is essential. The haemodynamicchanges in septic shock are very variable and are not specificfor the Gram status of the infecting organism. The earlystages of septic shock are often dominated by hypotensionwith relative volume depletion due to marked arteriolar andparticularly venular dilatation. Sufficient intravenous fluidshould be given to ensure that the intravascular volume isnot the limiting factor in determining global oxygendelivery. The type of fluid that should be administered andwhat constitutes ‘adequate’ volume resuscitation remaincontroversial. The response to therapy is crucial andfrequently unpredictable so it is not appropriate to use rigidprotocols. While the patient remains clinically volume-depleted, a continuous crystalloid infusion of at least1–2 ml/kg/hr should be given, together with full enteralnutrition if tolerated to achieve the planned 24-hourcrystalloid balance. Depending on haemoglobin concentra-tion, blood or synthetic colloid should be given as100–200 ml boluses to assess BP response to volume and toachieve CVP or PAWP targets. A recent meta-analysis hasconfirmed that albumin should not routinely be used in theresuscitation of critically ill patients (p. 425).

Excessive fluid replacement in pursuit of ‘supranormal’goals is not beneficial in patients with established organfailure (p. 184) and may be harmful, producing excessivetissue oedema.

Although ventricular function is frequently impaired, thecharacteristically low SVR ensures a high cardiac output(once the patient is adequately volume-resuscitated) albeitwith low blood pressure.

The choice of the most appropriate vasoactive drug to useshould be based on a full analysis of the circulation and

knowledge of the different inotropic, dilating or constrictingproperties of these drugs (Box 8.16, p. 192). In most cases a vasoconstrictor such as noradrenaline (norepinephrine) isnecessary to increase SVR and blood pressure, while aninotrope may be necessary to maintain cardiac output andprevent regional ischaemia. In the later stages of severesepsis the essential problem is at the level of the micro-circulation. Oxygen uptake and utilisation are impaired dueto failure of the regional distribution of flow and directcellular toxicity despite adequate global oxygen delivery.Tissue oxygenation may be improved and aerobicmetabolism sustained by reducing demand, i.e. metabolicrate (Box 8.27).

SPECIFIC THERAPIESCorticosteroidsAssessment of the pituitary–adrenal axis is difficult in thecritically ill but in some series up to 30% of patients haveadrenal insufficiency as assessed by baseline cortisol levelsand the response to adrenocorticotrophic hormone (ACTH).Corticosteroid replacement therapy is controversial; earlystudies using short-term, high-dose methylprednisoloneshowed no benefit but recent studies using lower-doseinfusions of hydrocortisone (8 mg/hr) for longer periods (5 days) demonstrated reduced vasoconstrictor requirementsin hyperdynamic sepsis and one study has shown an out-come benefit.

Activated protein CUntil recently, numerous large multicentre trials using anti-cytokine and other novel drug therapies to interrupt theinflammatory cascade had all produced disappointingresults. However, administration of activated protein C(levels of which frequently fall in critical illness) hasrecently been shown to produce a substantial reduction inmortality in patients with SIRS (Box 8.28).


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8.27 FACTORS THAT INFLUENCE METABOLIC RATE IN CRITICALLY ILL PATIENTS

● Fever (10–15% increase in V O2 for every 1°C rise)● Sepsis● Trauma● Burns● Surgery● Sympathetic activation (pain, agitation, shivering)● Interventions (e.g. nursing procedures, physiotherapy, visitors)● Drugs (e.g. β-adrenoceptor agonists, amphetamines, tricyclics)

N.B. Sedatives, analgesics and muscle relaxants will reducemetabolic rate.

8.28 ACTIVATED PROTEIN C IN SEVERE SEPSIS

‘Recombinant human activated protein C reduces 28-day mortalityin severe sepsis, even if multiple organ failure has alreadydeveloped.’● Taylor FB, et al. J Clin Invest 1987; 79:918–925.● Bernard GR, et al. N Engl J Med 2001; 344:699–709.

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SURVIVING SEPSIS CAMPAIGN

The Surviving Sepsis Campaign was launched in 2004 by aninternational group of critical care and infectious diseases‘experts’ representing 11 major organisations with the aimof reducing the worldwide mortality from sepsis by 25%within 5 years. After reviewing and grading the availableevidence, the group produced guidelines in the form ofpackages of care or ‘sepsis bundles’, each covering anaspect of the care of patients with severe sepsis (Box 8.4, p. 185). The belief is that this approach will eliminate thevariable and piecemeal application of new evidence. Theguidelines will be updated regularly as new evidenceemerges and both the implementation of the guidelines andthe outcome from sepsis will be audited to assess thesuccess of the initiative.

DISCHARGE FROM INTENSIVE CARE

Discharge is appropriate when the original indication foradmission has resolved and the patient has sufficientphysiological reserve to remain safe and continue his or herrecovery without the facilities available in intensive care.For long-stay ICU patients who have been ventilator-dependent, ‘step-down’ to the HDU is appropriate.Discharges from ICU/HDU should preferably take placewithin normal working hours as there is frequently a lack ofskills on the general wards and of suitable junior medicaland nursing support out of hours and at weekends.

The shortage of ICU and HDU beds in most hospitals in the UK creates pressure for early discharge but it has been shown that readmission rates and hospital mortalityincrease if discharge occurs prematurely or out of normalworking hours.

The critical care team should give the receiving team adetailed handover, provide a written summary with relevantrecent investigations, remain available for advice, andideally should visit the patient on the ward within the 24 hours after discharge.

WITHDRAWAL OF CARE

Withdrawal of support is appropriate when it is clear that thepatient has no realistic prospect of recovery or of survivingwith a quality of life that he or she would value. In thesesituations intensive care will only prolong the dying processand is therefore both futile and an inhumane waste ofresources. Nevertheless, when active support is withdrawn,management should remain positive and be directed towardsallowing the patient to die with dignity and as free fromdistress as possible. Patients’ wishes in this regard areparamount and increasing use is being made of advancedirectives or ‘living wills’. Communication with the patient,if possible, with the family, with the referring clinicians andbetween members of the critical care team is crucial (Ch. 1).Failure in this area damages working relations, causes stressand unrealistic expectations, and leads to subsequentunhappiness, anger and litigation.

BRAIN DEATH

The preconditions for considering brain-stem death and the criteria for establishing the diagnosis are listed on page 1187.

When formal criteria for brain-stem death are met it is clearly inappropriate to continue supporting life withmechanical ventilation and, at this stage, the possibility oforgan donation should be considered. All intensive careclinicians have a responsibility to approach relatives to seek consent for organ donation, provided there is nocontraindication to the use of the organs. This can be a verydifficult task but is easier if the patient carried an organdonor card. In the UK each region has a team of transplantcoordinators who can help with the process and will provideinformation and advice about the necessary tests.

SCORING SYSTEMS IN CRITICAL CARE

Admission and discharge criteria vary between units so it is important to define the characteristics of the patientsadmitted (case mix) in order to assess the effects of the careprovided on the outcome achieved (Box 8.29).

Two systems are widely used to measure severity ofillness:

● ‘APACHE’ II—Acute Physiology Assessment andChronic Health Evaluation

● ‘SAPS’ 2—Simplified Acute Physiology Score.

These scores include assessment of certain admissioncharacteristics (e.g. age and pre-existing organ dysfunction)and a variety of routine physiological measurements (e.g.temperature, blood pressure, GCS) that reflect the responseof the patient to his or her illness. Predicted mortality figuresby diagnosis have been calculated from large databasesgenerated from a range of ICUs. These allow a particularunit to evaluate its performance compared to the referenceICUs by calculating standardised mortality ratios (SMRs)for each diagnostic group:

SMR = observed mortality ÷ predicted mortality

A value of unity indicates the same performance as thereference ICUs while a value < 1 indicates a better thanpredicted outcome. A unit may have a high SMR in a certaindiagnostic category and this would prompt investigation intohow such patients were managed, with the intention ofidentifying aspects of care that could be improved.

When combined with the admission diagnosis, scoringsystems have been shown to correlate well with the risk of


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8.29 USES OF CRITICAL CARE SCORING SYSTEMS

● Comparison of the performance of different units● Assessment of new therapies● Assessment of changes in unit policies and management

guidelines● Measurement of the cost-effectiveness of care

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hospital death. Such outcome predictions can never be100% accurate and should be viewed as only one of manyfactors that the clinician considers when deciding whetheror not further intervention is appropriate.

COSTS OF INTENSIVE CARE

Measuring the costs of intensive care is complex. The most widely used system is the Therapeutic InterventionScoring System (TISS), which scores interventions andnursing activities for each day of admission and correlatesreasonably well with detailed measurements of staff,equipment and drug costs incurred within the unit. Since itfocuses on nurse-based interventions, TISS may also beused as an index of nurse dependency.

Current estimates of the daily cost of intensive care in theUK vary from £1000 to £2000, with high-dependency careaccounting for approximately 50% and general ward care20% of these costs. In the UK, less than 2% of total health-care expenditure is spent on critical care.

OUTCOME FROM CRITICAL CARE

The most widely used measure to assess outcome fromintensive care is mortality. This should be quoted at hospitaldischarge and at 28 days because mortality at the time ofdischarge from the unit will be influenced by the unitdischarge policy. Mortality is also influenced by case mix,length of stay and organisational aspects of the unit.

The Kings Fund has emphasised the need to demonstratelong-term benefit to justify the increasing costs of critical

care provision. Quality of life following discharge should beincluded in the evaluation of critical care but it is difficult tomeasure and interpret, not least because no objective pre-morbid assessment is possible with emergency admissions.However, several units in the UK now run follow-up clinicsand have identified that there is a high incidence of physicaland psychological problems affecting the patient and his orher family following ICU discharge.

FURTHER INFORMATION

Books and journal articlesBersten A, Soni N, Oh TE, eds. Oh’s intensive care manual. 5th edn.

Oxford: Butterworth–Heinemann; 2003.Davidson AC, Treacher DT, eds. Respiratory intensive care. London:

Hodder Arnold; 2002.Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis Campaign

guidelines for the management of severe sepsis and septic shock.Critical Care Medicine 2004; 32:858–873.

Fink M, Abraham E, Vincent J-L, et al, eds. Textbook of critical care.5th edn. London: WB Saunders; 2004.

Hillman K, Bishop G, eds. Clinical intensive care and acutemedicine. 2nd edn. Cambridge: Cambridge University Press;2004.

Hinds CJ, Watson D, eds. Intensive care: a concise textbook. 3rd edn. London: WB Saunders; 2004.

Webb AR, Shapiro MJ, Singer M, et al, eds. Oxford textbook ofcritical care. Oxford: Oxford University Press; 1999.

Websiteswww.esicm.org Guidelines, recommendations, consensus

conference reports.www.ics.ac.uk Clinical guidelines and standards for intensive

care.www.sicsebm.org.uk Intensive care evidence-based medicine

website. Reviews and critically appraised topics.www.survivingsepsis.org Surviving Sepsis website.

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